HSF1 and hepatocellular carcinoma: Thus, we found the following: (1) the oncogenic gain-of-function mutation in the RAS-MAPK signaling pathway increased HSF1; (2) increased HSF1 through RAS-MAPK signaling involved intracellular cholesterol homeostasis by activating the cholesterol biosynthesis pathway; and (3) KRIBB11, an HSF1 inhibitor, suppressed cholesterol biosynthesis and sensitized the antiproliferative effects of statin in HCC cells (Figure 6E).