Whereas the kinase activity of IRAK1 is dispensable for the capacity of mutant MyD88 to promote the survival of ABC DLBCL, NF-κB activation driven by oncogenic MyD88 mutations critically relies on the kinase activity of IRAK4, implicating this kinase as an interesting therapeutic target in lymphoid malignancies [40,50,51]. This evidence concerns the gene IRAK4 and diffuse large B-cell lymphoma.