In previous work, we found that CPSF1 is required for intronic polyadenylation in the AR gene, which is a pre-requisite for the splicing of alternative AR cryptic exons and the synthesis of truncated, constitutively active AR variants, including AR-V7.9 The current study extends this finding by demonstrating that CPSF1-dependent intronic poly(A) site selection is more widespread in prostate cancer cells than recognized from focused studies on AR. The gene discussed is AR; the disease is Familial prostate cancer.