Human short QT syndrome is diagnosed using the J point to T peak interval that may represent the interval between the end of the ventricular complex to the peak of the repolarisation wave.48 Short QT syndrome has been traced to HERG and other K+ channel mutations and more recently, Ca2+ channel function.49 The present findings are thus consistent with reported alterations in K+ conductance properties in the Pgc‐1β−/− system that would also modify current‐load matching.15 These changes appeared to result in shortened QTc intervals for mutant mice with adrenergic stress. The gene discussed is PPARGC1B; the disease is short QT syndrome.