On the other hand, through the combination of bioinformatics and cell biology, Li found that KRAS*‐STAT4‐mediated upregulation of Y chromosome KDM5D contributes substantially to the sex differences in KRAS* CRC by means of its disruption of cancer cell adhesion properties and tumor immunity, providing an actionable therapeutic strategy for metastasis risk reduction for men afflicted with KRAS* CRC. The gene discussed is STAT4; the disease is neoplasm.