Co-treatment of NSCLC cells with exogenous HA and triptolide completely abrogated triptolide-induced cytotoxicity and modulation of CD44, RHAMM, EGFR, Akt, ERK, caspase 3 and PARP levels, suggesting that targeting of HA-CD44/RHAMM signaling is the principal mechanism through which triptolide suppresses the proliferation and survival of NSCLC cells. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.