Previous studies have suggested that both IFNG and cytotoxic pathways are required to mediate allograft vasculopathy in calcineurin-treated mice.8,35 GZMB has also been shown to work together with PRF to induce endothelial cell apoptosis in the donor heart.36,37 We hypothesize that circulating CD38+HLA-DR+ CD8+ Tem cells infiltrate the intima of allograft arteries to cause intimal injury through proinflammatory and cytotoxic pathways, ultimately leading to CAV. The gene discussed is CD38; the disease is vascular disorder.