Chai et al. showed that YTHDF2 could promote the malignant progression of gliomas by accelerating UBX domain protein 1 (UBXN1) mRNA degradation via METTL3-mediated m6A modification [1]; Pan et al. verified that YTHDF2 could lead to the reduction of Tet1 mRNA decay by binding to m6A in Tet1 mRNA [47]; Hou et al. confirmed that the small ubiquitin-related modifier (SUMO)ylation of YTHDF2 could significantly increase the binding affinity of m6A-modified mRNAs and subsequently result in deregulated gene expression responsible for cancer progression [48]. The gene discussed is TET1; the disease is cancer.