Moreover, CFM-4 and its analog CFM-4.6 inhibited growth of TNBC and NSCLC cells in part by inducing apoptosis and stimulating activation of pro-apoptotic, stress-activated protein kinases (SAPKs) p38α/β and JNK1/2, caspase-8, and cleavage of PARP [12]. This evidence concerns the gene MAPK8 and non-small cell lung carcinoma.