Our results confirm prior findings showing STK11 and KEAP1 alterations each occur more frequently in KRAS altered vs WT tumors, whereas driver alterations across disease types tend to be mutually exclusive with KRAS. Of note, our findings of elevated co-alterations in MAPK/PI3K pathway genes among KRAS G13D mutated CRCs and endometrial cancers compared to G12D mutated tumors, further supports that KRAS G13D mutated tumors may present unique biochemical and clinical mechanisms26–28. This evidence concerns the gene STK11 and endometrial cancer.