U0126 and wortmannin each disrupted RIPC‐liver‐induced cardioprotection in Kcne2‐/‐ mice, such that postI/R arrhythmia incidence and severity were significantly increased in all inhibitor‐treated Kcne2‐/‐ mice, and VT durations prolonged, to levels similar to those of Kcne2‐/‐ mice without RIPC stimulus (P < 0.05, or P < 0.01 vs. RIPC‐treated Kcne2‐/‐ mice, Fig. 6A,B). The gene discussed is KCNE2; the disease is Arrhythmia.