C16:0 has been implicated as one of the key drivers of atherosclerosis by its uptake into the endothelial cell mitochondria membranes where they form channels and cause cytochrome-c release and induction of apoptosis.49 Further, ceramides cause endothelial dysfunction by decreasing nitric oxide (NO) production and by increasing NO breakdown by the formation of reactive oxygen species.31 These data suggest that a combination of elevated circulating levels of these ceramides, perhaps driven by C16:0, might cause an increase in vascular tone coincident with increased arterial stiffness. The gene discussed is CYCS; the disease is endothelial dysfunction.