In nasopharyngeal carcinoma, WTAP‐mediated m6A modification of DIAPH1‐AS1 enhances its stability via IGF2BP2, thereby promoting tumourigenesis and metastasis.[18] Similarly, METTL3‐mediated m6A modification facilitates OU6F2‐AS1 upregulation, driving colorectal cancer cell proliferation and lipogenesis.[19] In ESCC, m6A modification also plays a pivotal role, as FTO—highly expressed in ESCC—reduces the m6A methylation of LINC00022, preventing its degradation through YTHDF2 and thereby promoting ESCC cell growth.[20]. The gene discussed is DIAPH1; the disease is nasopharyngeal carcinoma.