Furthermore, the phytochemical triptolide inhibited the proliferation and survival of NSCLC cells having different genetic alterations, at least in part, by targeting members of the HA-CD44/RHAMM signaling pathway, thereby suppressing the expression and activation of downstream effector proteins, including EGFR, Akt and ERK and increasing the activation of pro-apoptotic proteins caspase 3 and PARP. This evidence concerns the gene EGFR and non-small cell lung carcinoma.