Although these findings identify inhibition of the CD40-CD40L dyad as promising therapeutic strategy in atherosclerosis, antibody-mediated inhibition of CD40 results in severe immune suppression, whereas antibody-mediated blockage of CD40L provokes thromboembolic events due to the disruption of CD40L-αIIbβ3 interactions in arterial thrombi [24]. The gene discussed is CD40LG; the disease is atherosclerosis.