The cooperative signal between stress hormones activating β2-adrenergic receptors and mutant EGFR results in inactivation of liver kinase B1 (LKB1), a tumor suppressor, and upregulation of IL-6, which leads to tyrosine kinase inhibitor (TKI) resistance in a T790M-independent manner in the treatment of NSCLC (Nilsson et al., 2017), suggesting that combinations of the well characterized and safely administered β-blockers with EGFR TKIs merit further investigation as a strategy to overcome drug resistance. Here, EGFR is linked to neoplasm.