A recent influential study found that mutation KRAS-STAT4-mediated upregulation of Y-chromosome KDM5D largely explains the sex difference in KRAS-mutated CRC (higher metastasis and mortality rates in male CRC) by disrupting the adhesion properties of cancer cells and tumor immunity, providing a viable therapeutic strategy to reduce the metastatic risk of CRC in men with KRAS mutations [28]. The gene discussed is KRAS; the disease is neoplasm.