In this regard, the demonstration of increased expression of genes encoding critical mediators of myocardial inflammatory injury, such as proinflammatory chemokines, SOCS3, and PTGS2, both in ToF and ASD after CPB is of particular relevance, suggesting that the development of therapeutic approaches that target these genes may be effective in controlling the inflammatory response triggered by CPB in patients affected by different CHDs. Here, SOCS3 is linked to atrial septal defect.