As AR and ERBBs70–73, and AR and Myc53–62, cross-regulate and reinforce each other to drive prostate oncogenesis and therapy resistance80,81, it is tempting to speculate that during PCa development and progression, the host, via producing androgens and ERBB ligands and activating AR and ERBB signaling, respectively, also upregulates LRIG1 in attempt to restrict unchecked oncogenic signaling and retard tumor growth (Fig. 10g). The gene discussed is AR; the disease is neoplasm.