In our study, ILK-MSCs treatment amounted to a 7.8% increment of LVEF compared with baseline, and reached by 10.3% when compared with vehicle in which LVEF progressively deteriorated and reduced by 2.5% at 22 days post infarction partially due to paucity of optimized pharmacological therapy such as angiotensin-converting enzyme inhibitor and beta-blockers41. This evidence concerns the gene ILK and infarction.