Neuroendocrine tumours are a heterogeneous group of tumours arising from a variety of specific chemical signalling cells in a range of organs. Superimposed on this intrinsic diversity of origin, they display a spectrum of biological behaviour from indolent well-differentiated tumours that may produce a variety of hormones, to aggressive poorlydifferentiated phenotypes that have rapid proliferation [1]. However, because of their collective rarity, they tend to get grouped into a single disease category for purposes of imaging and therapeutic trials. Peptide receptor radionuclide therapy (PRRT) is an evolving therapy but its utility is questioned by some because of the absence of prospective randomized controlled trials (RCTs). It sits amongst a growing number of therapeutic options, including pharmacological, hormonal [2] and liver-directed therapies, and surgical approaches. Pharmacological options include the mTOR inhibitor everolimus [3], the tyrosine kinase inhibitor sunitinib [4], and a variety of combination chemotherapy regimens, with promising results obtained with the combination of capecitabine and temozolomide in pancreatic NET in particular [5]. Amongst PRRT, there are also a myriad of options including a variety radioisotopes, different somatostatin analogues and combinations with radiosensitizing chemotherapy. Radiolabels include the Auger emitter In and the beta particle emitters Lu and Y; these have path-lengths of 0.02 – 10 μm, 0.8 – 1.5 mm and 5 – 12 mm, respectively. These can be administered alone or in combination, with emerging interest in alpha-emitters such as Bi. Somatostatin analogues include DOTA-TATE, DOTA-TOC and DOTANOC, with emerging interest in somatostatin antagonists such as pasireotide. Given this myriad of therapeutic strategies, how do we determine the optimal choice and sequencing of therapy in an individual patient? Should we rely on standardized approaches and RCTs to direct patient care, or is a personalized approach likely to be superior? In the current issue of EJNMMI, Romer et al. compare the outcomes in 1,051 patients treated with Y-DOTA-TOC or Lu-DOTA-TOC [6]. Median survival was 35.9 and 45.5 months, respectively, with no statistically significant difference between the groups. Treatment was individualized with Lu preferentially selected for patients with low tumour burden (up to three lesions), small lesions (diameter 90 μmol/l). This preselection of patients is quite appropriate based on theoretical considerations relating to the physical characteristics of these radionuclides and their differential potential for nephrotoxicity, but makes it difficult to draw robust conclusions between the two groups, as patients with more advanced disease and poorer prognosis were more likely to receive Y. Subgroup analysis adjusting for these confounders still suggested longer survival with Lu than Y. However, we would contend that the fact that individuals with a larger disease burden did not fare worse than those with less advanced disease supports a tailored approach of individualizing the chosen radioisotope properties to the burden of disease and patient comorbidities rather than indicating superiority of one over the other. The study adds to the growing literature supporting the use of PRRT. Despite a population that had been pretreated with surgery, chemotherapy and radiotherapy, the median survival M. S. Hofman : R. J. Hicks Molecular Imaging, Centre for Cancer Imaging, Peter MacCallum Cancer Centre, Melbourne, Australia