Although the underlying mechanisms are far beyond the scope of our work, this interference seems to involve the increased splenic β2-adrenoceptors-mediated production of interleukin 10 (Tian et al., 2018) in the early phases of myocardial infarction, as well as the high contribution of the spleen in the overall activity of angiotensin-converting enzyme (Swirski et al., 2009). This evidence concerns the gene IL10 and myocardial infarction.