This finding can be explained by the fact that, while in the first period following acute myocardial infarction Galectin 3 seems to be part of a survival mechanism to cope with the ischemic insult [10], actively contributing to the reparative processes in the infarcted area [12], in later time points, it supports the transition from acute to chronic inflammation and fibrosis. The gene discussed is LGALS3; the disease is myocardial infarction.