This idea is strengthened by observations that a specific de novo mutation in the TIR domain of MyD88 (L265P) leads to constitutive myddosome complexes driving aberrant NF-κB activation and inflammation in a number of B-cell human lymphomas (23), which to date has not been shown to be dependent on TIR domains from TLRs. This evidence concerns the gene NFKB1 and lymphoma.