In contrast, our study suggests that in patients with EGFR-mutant NSCLC receiving erlotinib, beta-blockers may confer additional benefits by modulating intracellular signaling pathways implicated in therapeutic resistance, such as MAPK and PI3K–AKT, downstream of EGFR activation [13,14,15]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.