Potential mechanisms that may contribute to the apparent greater sensitivity of patients with type IIb autoimmunity to BTK inhibition could include: lower density of surface FcεRI;41 weaker FcεRI activation by bivalent anti-FcεRI, relative to multivalent autoantigen–IgE complexes;42 lower levels of Syk, a BTK-activating kinase in the FcεRI pathway;43 and presence of autoantibodies that activate BTK-independent pathways (for example, anti-FcεRII) in patients without type IIb autoimmunity44,45. Here, BTK is linked to Autoimmunity.