Given that these PI3K and MAPK signaling pathways are upregulated during resistance, we hypothesized that overexpression of DARPP-32 proteins in EGFR-mutated NSCLC may promote EGFR:ERBB3 “bypass signaling” that enables tumor cells to evade EGFR TKI monotherapy. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.