Initiation of periodontitis generally necessitates the stimulation of the periodontal immune system through a bacterial dysbiosis, consequently setting complex inflammatory cascades in motion, characterized by the liberation of a variety of pro-inflammatory cytokines, mainly tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1 beta (IL-1β), IL-4, IL-6, IL-17 as well as interferon-gamma (IFN-γ) [1,2]. Here, IL1B is linked to periodontitis.