AKT1 and non-small cell lung carcinoma: We propose that by specifically inhibiting Akt together with EGFR, these otherwise diverse resistance mechanisms can be effectively controlled, allowing for a more rational and feasible treatment strategy to address both the molecular heterogeneity of EGFR-TKI resistance40 and the simultaneous presence of more than one mechanism of resistance (Supplementary Table 8) that we now know characterizes EGFR-TKI progression in many EGFR-mutant NSCLC patients.