NFKB1 and prostate neoplasm: As both MDSCs and activated NF-κB signaling are involved in the emergence of castration resistance (24, 25), our results highlight potential mechanisms of treatment resistance in PIN cells that enable evasion of cellular demise by Gemini-72, which may explain the limited chemopreventive and therapeutic efficacy of vitamin D. Nonetheless, treatment of prostatic tumors with vitamin D analogs may sensitize resistant cells to other anticancer agents.