In addition, in TKIs-sensitive cells, TKI can effectively reduce Erk1/2 and Akt phosphorylation, leading to NSCLC growth inhibition [77], while, in TKI-resistant cells, growth factor receptors or other growth promoting genes are often activated and serve as alternative pathways stimulating cancer cell survival [78]. The gene discussed is MAPK3; the disease is non-small cell lung carcinoma.