Moreover, more recent studies provide strong evidence to suggest that, in KRAS mutant tumor cells such as pancreatic ductal adenocarcinoma therapeutic synergism of targeting the glutathione antioxidant pathway is to be expected upon combination with inhibitors of the EGFR or AKT pathways [41], and therefore based on our data presented here future combination studies of EF24 with cetuximab of small molecule AKT inhibitors appear to be equally exciting. The gene discussed is AKT1; the disease is pancreatic ductal adenocarcinoma.