As RSF1 is overexpressed in both OS, NSCLC and PAAD, carcinogenic KRAS mutations are present in approximately 30% of human cancers and more than 90% of PAAD, RSF1 inhibition in OS and NSCLC cells inactivates the ERK signalling pathway [11, 14], which suggests that KRAS mutation-driven cancers with high protein levels of RSF1 increase sensitivity to cytotoxic drugs. This evidence concerns the gene RSF1 and pancreatic adenocarcinoma.