We propose that Akt inhibition, specifically, could more uniformly enhance response and survival in patients with high pAkt levels who are at high risk for Akt-mediated resistance, as this distinct approach has the unique potential to combat the otherwise profound heterogeneity of molecular resistance events that are present in EGFR-mutant NSCLC patients with acquired EGFR-TKI resistance to improve their outcomes. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.