KIT and heart failure: Thus, the origin of the increased number of c-kit+ CD34−CD45− cardiac cells and Ki-67+ cardiomyocytes with terminal heart failure was interpreted in several ways: i) activation of CSCs, which increases the total number and proliferative activity of the myocardium (5,13,14,19); ii) immigration of non-CSCs; iii) lack of differentiation of progenitor cells under pathological conditions and thus accumulation of juvenile cardiomyocytes; iv) dedifferentiation and expression of fetal and embryonic molecules of damaged adult cardiomyocytes.