While androgens play a role in AR activation, in our recent review, we discuss evidence that the AR, rather than androgens, is implicated in HCC progression and provide alternative mechanisms for AR activation, including mTOR crosstalk, lipogenesis-driven AR activity, CCRK-mediated activity, FAK-mediated signaling, and, most notably, AR splice variant (AR-SV) expression in HCC [3]. The gene discussed is PTK2; the disease is hepatocellular carcinoma.