A negative role of BTK in NLRP3 inflammasome activation is also supported by the evidence that Btk–/– mice exhibit increased severity of TNBS-induced colitis due to elevated IL-1β production, which may partially explain why XLA patients are prone to develop Crohn’s disease (Mao et al., 2020). Here, IL1B is linked to Bruton-type agammaglobulinemia.