To date, there is no clear evidence that describes the pathogenic role of a specific NKT subset during periodontitis; however, the ability of NKT1 and NKT17 cells to produce proinflammatory cytokines, specifically IFN-γ and IL-17A, respectively, broadens the conceptual paradigm that allows us to understand the pathogenesis of periodontitis. This evidence concerns the gene IL17A and periodontitis.