EGFR and non-small cell lung carcinoma: Using BH3 mimetics [20] with differential mitochondrial inhibitory activities, i.e. ABT-263 [21], ABT-199 [22, 23], and obatoclax [24, 25], we further tested the hypothesis that the EGFR TKI induced, TGFβ2-mediated mitochondrial prosurvival priming can be therapeutically targeted to prevent or eradicate the early adaptive drug escape in EGFR-mutant NSCLC.