However, these approaches are limited by the information available about drugs and diseases, so in our study, some assumptions had to be made: (i) most of the results relied on the expression and activity of MPL on non-megakaryocyte cell types, and (ii) our evaluation was made with the pathophysiological mechanisms of ITP described at the moment of the study, which could be improved in the future. This evidence concerns the gene MPL and autoimmune thrombocytopenic purpura.