Notably, the binding energies obtained (−7.8 and −7.7 kcal/mol for non-activated and activated AKT, respectively) and the dominance of hydrophobic contacts with limited hydrogen bonding are fully compatible with the physicochemical profile of 2,3′-dihydroxy-5′-methoxystilbene and with the micromolar concentrations required to experimentally reduce p-AKT/p-GSK3β levels and inhibit NSCLC cell viability, indicating good agreement between in silico predictions and observed biological activity. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.