In WM, culturing cell lines endogenously expressing MYD88L265P with an inhibitor of either MYD88 activation or IRAK1/4 significantly decreased nuclear staining of NF-κB p65, again indicating that MYD88L265P mediates its pro-survival effects through NF-κB signaling.9 In addition to NF-κB, both knockdown of MYD88 and use of an IRAK1/4 inhibitor diminished autocrine IL-6 and IL-10 signaling through STAT3 in MYD88L265P-overexpressing DLBCL cell lines, indicating that MYD88L265P regulates JAK-STAT3 signaling as well. This evidence concerns the gene STAT3 and diffuse large B-cell lymphoma.