At a molecular levels Btk has been shown to stabilise TNF-α mRNA via a p38- dependent pathway in X-linked immunodeficiency (Xid) mice and in XLA patients as well as being critically involved in NF-κB activation and specifically p65 phosphorylation downstream of multiple TLRs including TLR4, TLR7 and TLR9 [23]–[26]. The gene discussed is TLR4; the disease is Bruton-type agammaglobulinemia.