The remaining 10–15% of KRAS wild-type (KRAS-WT) tumors harbor frequent genomic events that can be targetable, such as homologous recombination genes, including BRCA1/2, PALB2, mismatch repair deficiency (dMMR), BRAF mutations/fusions, NRG1 and NTRK fusions, and other less common mutations [62]. Here, KRAS is linked to mismatch repair cancer syndrome 1.