It was around 1991, and David Easty – then a postdoc in my lab – had gone visibly pale. A friendly contact had mentioned that we were not after all the only people cloning protein tyrosine kinases from pigment cells; there was also one Richard Spritz. We knew of this Dr. Spritz, already in the forefront of pigmentary molecular biology. This was what Rich later called his ‘Lutz Giebel era’, when Giebel, Spritz and colleagues produced a rapid succession of high-impact papers that among other things identified the tyrosinase gene as the locus for human oculocutaneous albinism (OCA) types 1A and 1B, and the KIT gene as the locus for human piebald syndrome. So he was the last person our tiny band wanted to be competing with. ‘Bother!’ (or something like that), said David. Maybe a year later the phone rang, and there, still more alarmingly, was the same Dr. Spritz wanting to talk. ‘Is this’, I ventured, ‘about tyrosine kinases?’ It was not (although the question led to useful discussions on that topic, too). Instead, that phone-call was to begin a long, stimulating and productive series of collaborations, and a lasting friendship. Rich actually wanted to discuss a gene for human OCA type 2, and its orthology with p (pink-eyed dilution) in the mouse. He had the idea of using cultured p-null mouse melanocytes to test for functional complementation by a human P cDNA and for dysfunction with mutations from OCA2 patients. And could we isolate the melanocytes? Which, ultimately, we did, and the complementation idea worked. It was later extended to other pigmentary loci. Richard Spritz, MD, began his research career with Sherman Weissman at Yale, where the first human genes were being cloned and sequenced: globin genes. Rich was lead author on the paper identifying the first mutation, in a globin gene from thalassemia – exciting times to enter molecular biology. More fundamental research followed; but after getting a faculty position at Wisconsin (1981), Rich turned to something even more interesting (as readers of this journal will agree): pigmentation. Thus began the TYR and KIT work, with extensive molecular studies of albinism and piebaldism. Then came cloning and pathology of P/OCA2, studies of genomic SILV/PMEL, and a burgeoning interest in a large set of pigmentary genes that proved pivotal in animal cell function. These were the HPS (Hermansky–Pudlak syndrome) genes, all regulating the correct routing of proteins to cellular organelles, including melanosomes. The Spritz group and collaborators published the sequences for HPS1 and the related CHS/LYST in two Nature Genetics papers in 1996, followed by many papers on further HPS genes and their mutations in patients. Meanwhile, I was attending the medical advisory panel of the UK Vitiligo Society. The panel thought that someone should study the genetics of vitiligo. ‘I know just the person’, I proposed, ‘Richard Spritz’. Now Rich wasn’t keen on this idea initially, since vitiligo was inherited in a non-Mendelian manner, which threatened some complicated and messy genetics. But he eventually became interested, partly by the disorder’s common and distressing nature and the huge enthusiasm of the patients for research. Rich took a trip to England in 1997, driving around the country with me or co-workers, meeting patients and collecting blood samples. That visit included the occasion when we stopped for lunch at a country pub and Rich, to sample something typically English, opted for steak and kidney pudding. The pudding arrived, looking small, pale, glutinous and suspiciously tin-shaped. Rich valiantly chewed his way through it, while I felt internationally embarrassed. (Still, the beer was OK.) At any rate, those blood samples provided the basis for a successful NIH grant application by Rich, with quantitative geneticist Pam Fain, beginning the mammoth collaborative vitiligo genomics study that now involves dermatologists and patients worldwide. In more high-impact publications, at least 17 vitiligo susceptibility genes have now been identified, nearly all encoding elements of the immune system. Two of Rich’s favourite occupations are mountaineering and skiing, so he and Diana were delighted to move in 1998 to the University of Colorado at Denver, within easy reach of the Rocky Mountains. There, as Director of the Human Genetics program, Rich continues to inspire students and young researchers to perform rigorous and elegant genetic studies. These are mostly on pigmentary disorders, although little sidelines like diabetes and cleft palate sometimes creep in. He contributes extensively to charity advisory boards and NIH panels, and also as a member of the PASPCR Council and the PCMR editorial board. He continues to collaborate widely and to benefit many colleagues’ research with his incisive thoughts and exacting standards. He is truly an outstanding leader in human molecular genetics, and irreplaceable in our pigmentary field, where his extraordinary impact on progress shows no sign of diminishing.