(157) found that treatment of a dalafenib-resistant (GSR) cell line (V600E NSCLC) with dalafenib resulted in upregulation of EGFR, activation of the EGFR-RAS-CRAF pathway, and sustained activation of ERK1/2, enhancing EGFR-mediated RAS activity. This evidence concerns the gene EGFR and non-small cell lung carcinoma.