Taken together, these results imply that c-MYC and AP4 promote cholesterol synthesis and cancer cell proliferation through the induction of SQLE. The elevated cholesterol levels in p53-deficient CRC cells with high c-MYC expression presumably increase their dependency on cholesterol, which could explain the increased sensitivity of these cells to SQLE inhibition. This evidence concerns the gene TFAP4 and colorectal carcinoma.