These results are in agreement with the well-established pathogenic role of Th1 cells and IL-6 in TAC-induced HF, since SOCS1 and SOCS3 inhibit IFNγ signaling, and IL-6, respectively,44,45 and further support an anti-inflammatory role of tryptophan/AhR axis in cardiac inflammation induced by TAC. This evidence concerns the gene IFNG and persistent truncus arteriosus.