For some, melanocytes are an end in themselves; a wonderful cell type that gives colour to life. For others, with a different perspective, melanocytes represent a window on a wider world where this lineage provides a model system to address broader issues relevant to life in general. The importance of melanocytes as a model system is highlighted by the numbers of News and Views published in this journal on papers published in high profile journals. Whereas perhaps 20 years ago muscle development was fashionable, these days one cannot escape the feeling that this is the age of the melanocyte. Melanocytes really have become the New Black. The usefulness of the lineage as a model system is highlighted in two reviews in this issue. Mireille van Gele et al profile Griscelli syndrome, while Vladislava Melnikova and Menashe Bar Eli highlight the role of inflammation in melanoma metastasis. Melanocytes, can be classed as secretory cells in which the process of genesis of the melanosome, its transport along dendritic processes, and ultimate export to surrounding keratinocytes has parallels to the generation and release of secretory granules from other tissues. The use of melanocytes to study the secretory process has advantages over other cell types in that defects in any step of the secretory pathway that lead to failure of melanosomes to end up in the correct destination in the right numbers gives an obvious pigmentation phenotype. This has meant the genetics of pigmentation has revealed a wide range of genes implicated in the development and function of the melanocyte lineage including genes intimately involved in melanosome transport. Because melanosomes use machinery that in other cell types may be recruited to transport vesicles, the lessons learned from studying defects in melanosome transport have given key insights into vesicle transport in general, and in particular into the molecular defects underpinning Hermansky-Pudlak and Griscelli syndromes. The autosomal recessive and early onset Griscelli syndrome is characterised by mutations in the Rab27a, myosin 5a and melanophilin genes, that in addition to affecting pigmentation may also affect neurological and immune system function. The mutations underpinning this syndrome, and their effects on the mechanisms underlying vesicle and melanosome transport are the subject to a comprehensive review by van Gele et al. While melanocytes may represent good models for understanding vesicle transport, melanoma is an excellent model for cancer. Unlike many cancers where symptoms present after the disease has progressed to a stage where metastasis has already occurred, as a skin cancer, all stages of melanoma are amenable to study, including the normal melanocyte, nevus, radial and vertical growth phases and metastasis. One of the major areas of interest in melanoma, and for that matter in cancer research in general, is the process of metastasis, as the majority of cancer-related deaths arise through colonization of sites distant from the primary tumour. In this respect, melanoma is particularly interesting as it has a notorious propensity to metastasise early. Although the standard model of metastasis proposed for many cancers involves the accumulation of ‘pro-metastasis’ genetic lesions, increasing evidence suggests that early stage melanoma metastasis may be driven by mechanisms in which the effects of the miroenvironment superimposed on pro-proliferation genetic mutations in BRAF for example, lead to adoption of an invasive phenotype. In addition to hypoxia and nutrient deprivation, one of the major micoenvironmental influences within a tumour will be the effects of inflammation and infiltration by cells of the immune system. In a timely review, Melnikova and Bar Eli discuss the mechanisms by which an inflammatory response can affect the metastatic potential of melanoma and its therapeutic implications.