Until recently, a genome‐wide CRISPR/Cas9 screen identified GOLGA7 as a unique synthetic lethal gene in NRAS‐mutant leukemia cell lines.[32] Later, our study also revealed that GOLGA7 specifically sustains the proliferation and survival of human cancer cells driven by NRAS mutations, but not those with KRAS mutations.[31] In this study, we recapitulated similar results in mice, demonstrating that the loss of Golga7 inhibited the oncogenic Nras signaling pathway within BM cells. This evidence concerns the gene KRAS and cancer.