A phase I/II clinical trial has revealed that DLBCL patients having both CD79B and MYD88 mutations were more responsive to the BTK inhibitor ibrutinib, whereas CARD11 mutations and TNFAIP3 inactivation (TNFAIP3 nonsense or frameshift mutation, TNFAIP3 double deletion, or low TNFAIP3 mRNA expression) were associated with inferior responses to ibrutinib [59]. Here, MYD88 is linked to diffuse large B-cell lymphoma.