Prolonged overproduction of IFN‐I is implicated in the pathogenesis of periodontitis.16, 17, 18 Through association with IFNAR1, the TAM receptors can activate SOCS1/3 to inhibit IFN‐I production.15 The first evidence for the involvement of the TAM signalling in the development of periodontitis came from a recent study showing that the unrestrained IFN‐I production following P gingivalis infection was due to down‐regulation of TAM components.19 Specifically, repeated oral infections with P gingivalis led to MYD88 degradation and a reduced expression of Gas6, Axl and Pros1 regulated by MYD88. The gene discussed is IFNAR1; the disease is periodontitis.