For instance, the study by Keck et al. points out inflammation arising from cardiac resident CD11b/c cells as a potential trigger of TNFR2- and ORAI3-dependent protective signaling pathways in cardiomyocytes, promoting early adaptive hypertrophy, improving resistance to oxidative stress, and delaying transition to HF, in response to TAC-induced pressure overload or β-adrenergic chronic infusion [131]. This evidence concerns the gene TNFRSF1B and hydrops fetalis.