The purpose of this study was (1) to investigate whether chronic administration of a KATP channel agonist, nicorandil, results in attenuated myocardial fibrosis through regulation of M2 and myofibroblast accumulation, and (2) to assess the role of RhoA/ROCK in cardiac fibrosis in a rat MI model using a ROCK inhibitor, fasudil (1‐(5‐isoquinolinesulfonyl)‐homopiperazine). The gene discussed is RHOA; the disease is myocardial infarction.