In DLBCL tumors, it is known that MYD88L265P promotes cell survival through its spontaneous assembly into a complex with IRAK4 and IRAK1, leading to IRAK1 phosphorylation and NF-κB activation.10 However, the correlation between MYD88L265P and the activation of downstream signaling pathways or cell growth and survival has not been investigated in WM. The gene discussed is NFKB1; the disease is diffuse large B-cell lymphoma.