Overall, these data suggest that NXP800, through a novel mechanism of action, offers the potential for clinical antitumor activity against prostate tumors not only with AR splice variant expression but also with high E2F and MYC activity, supporting clinical evaluation following progression on the first AR-targeting therapy in which both AR-dependent and AR-independent mechanisms of resistance have emerged (6–14, 80). The gene discussed is AR; the disease is prostate neoplasm.