Notably, we observed the inhibition of EGFR phosphorylation together with the inhibition of downstream signaling molecules in the MAPK/ERK and PI3K/AKT pathways in H1993-MTA cells, which carry wild-type EGFR. Furthermore, although both FGF2 and FGFR1 demonstrated a marked increase in H1993-MTA cells, the downstream signaling molecules in the MAPK/ERK and PI3K/AKT pathways remained inhibited in these cells, which cannot readily be explained by the activation of alternative bypass track theory presumed in the EGFR mutant NSCLC cell lines [14, 34]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.