Considering the results indicating that (1) MYC is a well-known oncogene that triggers the expression of target genes to benefit cell proliferation, cell survival, and stemness maintenance and (2) AFF4 and NF-κB are known to regulate MYC expression, through which NF-κB signaling enhances the proliferation and survival of cancer cells during the development and recurrence of BlC, it can be speculated that m6A modification by METTL3 affects the AFF4/NF-κB/MYC signaling network to regulate BlC progression20. The gene discussed is AFF4; the disease is cancer.