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. The gene discussed is GOLGA7; the disease is cancer.