The intriguing activation of p38α/β SAPK however in the untreated drug-resistant NSCLC cells as well as in the parental or TKI-resistant NSCLC cells that were treated with CFMs (see Figure 3 and Supplementary Figures 1 and 3) would suggest for known biphasic growth and stress signaling roles, respectively, of p38α/β kinase. This evidence concerns the gene MAPK9 and non-small cell lung carcinoma.