First described in activated B-cell (ABC)-like subtype of diffuse large B-cell lymphoma (DLBCL) [where it occurs in 21% of patients (15)], the MYD88L265P mutation constitutively activates NF-κB and JAK kinase signaling through TLR9, IRAK1 and IRAK4 (16, 17), and independently through BTK (18), conferring a pro-survival advantage to mutated B cells. This evidence concerns the gene BTK and diffuse large B-cell lymphoma.