To evaluate the association between KRAS mutational status and the senescence-like sate as mediator of resistance in PDAC, we first determined the capability of the chemotherapeutic drugs, gemcitabine, 5-fluorouracil (5FU), oxaliplatin, SN38 (the active metabolite of irinotecan), and paclitaxel at 0.1 and 1 μM to induce therapy-induced senescence-like in three commercial pancreatic cancer cell lines (CCL) with different KRAS status. This evidence concerns the gene KRAS and familial pancreatic carcinoma.