Compensatory hypertrophy at cellular level is expected to occur in the remote area after MI, however no signatures of cardiac hypertrophy were detected at gene level {i.e., activation of fetal gene program, decreased expression of FAO enzymes in favor of glycolytic ones, up-regulation of signaling pathways involved in hypertrophy [as PI3K, AKT, AMP-activated protein kinase, and mTOR (21)]}. This evidence concerns the gene MTOR and cardiac hypertrophy.