KMT5A and cancer: Abnormal expression of SETD8 has been reported in various cancers, though the mechanisms remain poorly understood.[24] Previous studies have emphasized the role of ubiquitin‐mediated degradation in SETD8 regulation, with E3 ligases like APCCdh1,[25] SCFSKP2,[26] CRL4Cdt2,[27] and SCFβ‐TRCP[28] shown to mediate SETD8 proteolysis.