Reperfusion of ischemic myocardium induces substantial cellular injury resulting from mechanical and biochemical necrotic injury (Honda et al. 1047; Piper et al. 2004; Halestrap 2006), which involves substantial Ca2+‐loading during ischemia, driven by the “coupled exchanger” mechanism between the sodium/hydrogen exchanger (NHE) and sodium/calcium exchanger (NCX) (Tani and Neely 1989; Allen and Xiao 2003). The gene discussed is TLX2; the disease is ischemia.