In HCC derived from nonalcoholic steatohepatitis (NASH), androgen receptor (AR)‐driven oncogene cell cycle‐related kinase (CCRK) induces STAT3‐AR promoter co‐occupancy and transcriptional upregulation, leading to GSK3β phosphorylation, activation of the mTORC1/4E‐BP1/S6K/SREBP1 cascade, and enhanced recruitment and tumorigenicity of MDSCs [232]. Here, SREBF1 is linked to metabolic dysfunction-associated steatohepatitis.