Therefore, on the basis of : i) the idea that in the progression of the cellular and molecular events that characterize acute MI, the platelets generated around the acute event might be characterized by a specific profile of gene expression; ii) our previous works on PKCε expression during MK differentiation [34], [35] and erythroid differentiation [36], [37]; iii) the functional data on platelet PKCε available in the mouse, we hypothesized that an ectopic expression of PKCε might be present in platelets from MI patients. This evidence concerns the gene PRKCE and myocardial infarction.