Loss of function of negative regulators was more prevalent in MYD88 with CD79A/CD79B activating mutations, than in MYD88 lacking CD79A/CD79B alterations (56% vs 36.4%) which is of potential clinical utility because aggressive lymphomas with MYD88L265P and CD79B mutations have a response to ibrutinib (Bruton’s tyrosine kinase is downstream of BCR) and presumably have chronic active BCR signaling (Shaffer et al., 2006; Puente et al., 2015; Chapuy et al., 2016; Schmitz et al., 2018). The gene discussed is MYD88; the disease is lymphoma.