The following observations were made: (a) miR‐200c acted as a new pro‐hypertrophic miRNA; (b) the down‐regulation of miR‐200c inhibited cardiomyocyte apoptosis and reduced the production of ROS; (c) miR‐200c directly targeted MLCK; (d) the suppression of miR‐200c ameliorated CH via activation of the MLCK signalling pathway. This evidence concerns the gene MYLK and cyclic hematopoiesis.