Excitingly, our finding that St2Stect/Asymkindimer sub-units are epidermal growth factor (EGF) ligand high affinity binding sites, which are the sites previously proposed to drive tumor growth under pM physiological ligand concentrations49, explains how the dysregulation of the ligand-free kinase active state by NSCLC mutations translates into their ability to potentiate EGFR-dependent tumor growth in vivo. The gene discussed is EGFR; the disease is neoplasm.