EGFR play a central role in the pathogenesis of NSCLC, and therapies modulating EGFR-associated signalling pathways have demonstrated clinical potential in improving treatment outcomes beyond conventional cytotoxic approaches.26 Drugs predicted to bind the allosteric site of EGFR-TK may influence downstream signalling cascades and potentially modulate cellular function.27 The allosteric site has attracted significant interest from researchers and is now regarded as a highly promising target for developing anti-NSCLC drugs. The gene discussed is TKT; the disease is non-small cell lung carcinoma.