KRAS and pancreatic adenocarcinoma: However, the finding that EFR3A specifically binds KRAS in the active GTP-bound state and that sgEFR3A did not affect the growth of HEK-HT cells in the absence of oncogenic KRAS or in the KRAS wild-type pancreatic adenocarcinoma cell line BxPC3 supports, but admittedly does not prove, that it is the recruitment of EFR3A to KRAS that is a key step in the ability of EFR3A to promote oncogenic KRAS signaling.