Although the prognostically rather poor MCD subtype, which comprises the majority of MyD88-mutant cases (specifically those with the most prevalent L265P mutation)75, displayed limited association with DC/PU.1 signatures (Supplementary Fig. 8b), we decided to more deeply investigate lymphomas with mutant MyD88, because this toll-like receptor adaptor molecule reportedly operates upstream of AP-1/JUN77. This evidence concerns the gene JUN and lymphoma.