IL6-driven endothelial inflammation is a well-documented axis associated with cardiovascular risk after kidney transplantation and blockade of the IL-6/IL6-R signaling pathway has been evoked as a means to limit the harmful effects of inflammation in experimental studies Our study also further supports that risk factors associated with marginal donors such as aging, hypertension, and a history of stroke could further sustain fractalkine-mediated endothelial activation and leucocyte recruitment and impact transplant vascular injury and repair and kidney and heart transplant rejection (34, 35). The gene discussed is IL6R; the disease is cardiac transplant.