Some of these are dependent on the inhibition of TAp63, but others reflect the ability of mutant p53 to regulate other proteins and transcription factors such as SREBPs, NF-Y, SP-1, or VDR (20, 46–48), through which mutant p53 can promote cell proliferation, chemoresistance, cholesterol metabolism, and various other tumor-promoting processes. This evidence concerns the gene VDR and neoplasm.