In diverse microenvironments, Burra Anand et al. demonstrated that METTL3 mediates m6A modification in human gingival fibrocytes within the periodontitis, leading to an increased expression of pro-inflammatory factors such as triggering receptor expressed on myeloid cells-1 (TREM-1), interleukin (IL)-1β, and IL-6, which promote the progression of periodontitis [140]. This evidence concerns the gene METTL3 and periodontitis.