Among m6A readers, YTHDF1, a YTH domain protein, drives the translation of m6A-modified mRNAs by interacting with translation initiation factors.15 Notably, YTHDF1 stands out as the top upregulated m6A regulator in CRC, with studies linking it to tumor growth, metastasis, and the modulation of antitumor immunity in a m6A-dependent manner.13,16 Recent reports have also implied that YTHDF1 promotes cancer stemness, tumorigenesis, and chemoresistance.17–19 Nevertheless, the CSC-specific role of m6A modification in CRC remains underexplored. The gene discussed is YTHDF1; the disease is neoplasm.