Their most relevant finding was that the rabbit cardiomyocytes, whose mitochondria housed relatively higher concentrations of high-affinity IF1, were more effective at preserving ATP during short bouts of ischemia than rat and pigeon hearts, whose cardiomyocytes contained lower levels of high-affinity IF1 and a full complement of lower-affinity IF1, respectively [6]. The gene discussed is ATP5IF1; the disease is ischemia.