Since ILK is a protein Ser/Thr kinase that causes phosphorylation of Akt/PKB on Ser473 and glycogen synthase kinase-3β (Gsk-3β) on Ser9[11], and the ILKR211A mutation is thought to be either null or inhibitory to canonical ILK signaling[6,7,13], we measured the phosphorylation status of these ILK prosurvival targets in border zone of post-MI myocardium. This evidence concerns the gene GSK3B and myocardial infarction.