In diffuse large B-cell lymphoma (DLBCL) with the MyD88 L265P mutation caused by TIR domain mutation, studies have found that the histone deacetylase inhibitor panobinostat reduces the binding of STAT3 to the MyD88 promoter by inhibiting STAT3 phosphorylation, thereby downregulating MyD88 expression, and when combined with the BTK inhibitor ibrutinib, it more potently suppresses NF-κB activity and has been shown to induce tumor regression in DLBCL xenograft models (233). Here, BTK is linked to neoplasm.