Due to its central role in ischemia/reperfusion injury, the NHE has previously been suggested as an end‐effector of IPC (Gumina et al. 2001; Yellon and Downey 2003), even though the conditions resulting from ischemia/reperfusion, seem likely to stimulate NHE activity (Kandasamy et al. 1995; Haworth et al. 2003). Here, SLC9C1 is linked to ischemia.