UGT2B17 was shown to stimulate cancer cell proliferation, invasion and progression to castration-resistant PCa in a mouse xenograft model after prolonged androgen deprivation.44 In this study, the action of UGT2B17 was mediated by the activation of the c-Src kinase, enhancing ligand-independent AR signalling.44 However, in the latter study, the correlation between UGT2B17 tumour expression and clinical outcomes was not evaluated in men with PCa. Here, CSK is linked to neoplasm.