Background: The c-kit receptor has been known as a proto-oncogene, cell specific isolated maker of stem cell, promoter of cardiac stem cell differentiation, and regulator of cardiomyocyte maturation. However, the pathophysiologic role and the regulation factor of c-kit in the myocardium is still not determined. We hypothesized that c-kit receptor may contribute to myocardial protection against ischemic condition. Methods and Results: The c-kit expression was observed in the rat neonatal cardiomyocytes (rCMCs) and rat heart under ischemic condition. Normal condition, c-kit was detected at cytoplasm of rCMCs. However, it was not detected in the normal myocardium of rat heart. At serum starvation condition, c-kit was detected at circumference of nucleus of rCMCs. At hypoxic condition, c-kit was detected at both circumference of nucleus and cytoplasm of rCMCs. Myocardial ischemia-reperfusion injury (IRI) was induced by left anterior descending coronary artery ligation for 1 hour and followed by reperfusion. At 24 hours after IRI, c-kit was detected at circumference of nucleus and around the gap junction in the myocardium. The cells having c-kit expression at the circumference of nucleus was defined as cardiomyocytes stained by anti-troponin-I Ab stain. The c-kit expression was detected around the gap junction, but not localized perfectly into the gap junction stained by anti-connexin Ab. Conclusions: In this study, c-kit receptor may be an early protection factor against ischemic condition. More information of the c-kit expression in the in vitro study and infarct myocardium will be elucidated.