In this study, we addressed this enigma by showing in the male NAFLD context (Figs. 1 and 2) that IL-6 can induce a self-reinforcing STAT3/AR/CCRK oncogenic circuitry, in which CCRK facilitates the physical interaction of phosphorylated STAT3 and AR and their co-occupancy at CCRK promoter for sustained transcriptional activation (Fig. 3). This evidence concerns the gene AR and metabolic dysfunction-associated steatotic liver disease.