Elevated levels of IFN‐ were detected in gingival tissues and plasma of periodontitis patients.16, 17 Moreover, the periodontitis‐associated pathogen P gingivalis or its LPS (p.g‐LPS) can stimulate IFN‐ production by macrophages through TLR signalling.18 Interestingly, loss of negative regulation on IFN‐I by TAM was reported to be responsible for the uncontrolled IFN‐1 production in a murine model of P gingivalis‐induced periodontitis,19 supporting a protective role of the TAM signalling against this oral inflammatory disease. Here, IFNA1 is linked to periodontitis.