Taken together, these data confirmed that treatment with NXP800 suppresses AR signaling and provided novel insights into the mechanism of action of NXP800 in prostate cancer cells, with activation of the UPR and inhibition of AR, MYC, and E2F activity—all reported to be key to the development and progression of CRPC (5, 64–66). The gene discussed is MYC; the disease is prostate cancer.