In conclusion, apoptotic resistance and the heterogeneity of pancreatic tumors have been outsmarted by a widespread normalization of overexpressed anti-apoptotic genes and the inhibition of KRAS. By silencing of the activated KRAS and members of the apoptotic resistance pathway, we were able to induce apoptosis and proliferation inhibition in a broad spectrum of pancreatic cancer cells with our SGS6, in vitro as well as in vivo. This evidence concerns the gene KRAS and familial pancreatic carcinoma.