Moreover, we show that loss of EFR3A, EFR3B, or PI4KA all reduce short-term (Titer-Glo analysis) and long-term (colony formation) 2D-transformed growth, as well as 3D growth-transformed growth (soft agar) in not only oncogenic KRAS-transformed HEK-HT cells, but also in multiple human pancreatic adenocarcinoma cell lines characterized by an endogenous mutant KRAS allele. This evidence concerns the gene EFR3B and pancreatic adenocarcinoma.