As expected, RIPC‐limb‐treated Kcne2‐/‐ mice were less susceptible to postI/R arrhythmia compared to nontreated Kcne2‐/‐ mice, as seen in Figures 3 and 7A. However, pretreatment with wortmannin eliminated the antiarrhythmia effect afforded by limb preconditioning. The gene discussed is KCNE2; the disease is Arrhythmia.