The combination of effects we observed using the Arrhythmia model, i.e., abrogation by ERK1/2 and GSK-3β inhibitors both of RLIPC-induced anti-arrhythmic cardioprotection, and of ERK1/2 and GSK-3β Ser9 phosphorylation, directly implicates a pathway involving these two proteins in anti-arrhythmic effects of RLIPC. The gene discussed is MAPK3; the disease is cardiac arrhythmia.