m6A modification affected dental pulp inflammation via regulating the splicing of MyD88 transcript, and knockdown of m6A demethylase FTO promoted inflammatory responses of cementoblasts.[25, 45] Our previous study predicted the potential role of m6A‐associated single‐nucleotide polymorphisms (SNPs) in the pathogenesis of periodontitis.[26] However, there is still a paucity of research regarding the precise role of the m6A modification in inflammatory oral diseases. Here, MYD88 is linked to periodontitis.