Targeted genome editing to abrogate constitutive production of IL30 also led, in both AR+ and AR− human PC cell types, to the downregulation of a wide range of oncogenes, including AR, the main driver of castration-resistant PC development and of acquired resistance to androgen deprivation therapy, and ERG, which is overexpressed in a high proportion of PCs, due to a gene fusion with the androgen-driven promoter of the TMPRSS2 gene [68]. The gene discussed is TMPRSS2; the disease is pachyonychia congenita.