Remarkably, SpiD3 attenuated NFκB activation in the presence of soluble CD40 ligand (sCD40L), a known activator of both canonical and noncanonical NFκB pathways (ref. 35; Supplementary Fig. S6B), suggesting SpiD3 disrupts supportive CD40L-dependent T cell–mediated interactions in CLL (35). The gene discussed is CD40LG; the disease is B-cell chronic lymphocytic leukemia.