In current study, we further demonstrated the underlying mechanisms by which the co-suppression of PKC α and β appeared essential for the viability of pancreatic cancer cells harboring mutated K-ras or prostate cancer cells expressing active Akt. The data suggested that these two PKC isoforms coped with aberrant Ras or Akt to keep the homeostasis in the cancer cells. This evidence concerns the gene PRRT2 and familial pancreatic carcinoma.