Equivalent amounts of prostates/tumors (20%; n = 2/group) developed into poorly differentiated/neuroendocrine (PD/NE)-like cancers in both cohorts and prostate/tumor weights as well as Ki67 staining were not significantly different between cohorts (Figure 2B–D; Supplemental Figures S4 and S5A) at 30 weeks, indicating that CAMKK2 inhibition did not increase (or decrease) ADT-mediated long-term protection against cancer progression in the context of localized PD/NE tumors. The gene discussed is CAMKK2; the disease is cancer.