Thus, future efforts that interrogate whether therapeutic manipulation of IL-6-STAT4 efficiently prevents proarrhythmic signatures (ion channel function, APD phenotypes, QT prolongation, VT/SCD vulnerability) in diseased HFD/obese ventricular tissues/myocytes, thus counteracting the redundancy of cytokines and undesired side-effects elicited by breaching the essential homeostatic role of classical IL-6 signaling, are likely to be rewarded with novel therapeutic perspectives and beneficial translational implications in patients. This evidence concerns the gene STAT4 and Schnyder corneal dystrophy.