Mechanistically, STAT3-AR co-binding stimulated by CCRK transcriptionally activates its own promoter, which in turn triggers the mTORC1/4E-BP1/S6K/SREBP1 cascades via GSK3β phosphorylation to augment hepatic lipid accumulation, glucose intolerance, insulin resistance, and tumorigenicity. The gene discussed is STAT3; the disease is Glucose intolerance.