Therefore, suppression of mTOR in specific KRAS-dependent PDAC subtypes leads to the impediment of tumorigenesis and furthermore, over 90% of PDAC patients have oncogenic KRAS mutations; thus, suppressing the p53/REDD1 axis as a molecular central target, may increase metformin’s potential anti-tumor effect to become a novel promising chemotherapeutic agent in the foreseeable future [68,69]. This evidence concerns the gene KRAS and neoplasm.