Given the absence of the MYD88 mutation in the transformed sample, it is difficult to ascribe this initial response to effectiveness of that therapy in all stages of LPL as opposed to representing a case of the known phenomena of ibrutinib response in non‐GC DLBCL and the possibility that the LPL and DLBCL in that sample arose from the same ancestral clone through activation of different pathways [11]. This evidence concerns the gene LPL and diffuse large B-cell lymphoma.