While B-cell lymphoma cells with constitutively active MyD88L265P contain the cleaved MyD88 fragment in the absence of additional stimulation, those cells have a unique ability to escape this negative regulation mechanism, as the mutated TIRL265P domain resulting from the proteolytic cleavage is no longer inhibitory and can in contrast even support signaling in the presence of full-length MyD88. The gene discussed is MYD88; the disease is B-cell non-Hodgkin lymphoma.