Our findings provide evidence of FAK-YAP/TEAD signaling engagement in drug-tolerance across EGFR-mutant, ALK fusion-positive, KRAS-mutant, and NF1-mutant NSCLC more broadly and therefore offer rationale for combinatorial treatment approaches testing FAK inhibitors (e.g., VS-4718) and TEAD inhibitors (e.g., VT104/VT108) across several molecularly defined NSCLC subtypes to enhance treatment response to targeted inhibitors against these important oncogenic targets. The gene discussed is NF1; the disease is non-small cell lung carcinoma.