IL6 and Ventricular arrhythmia: Therefore, future efforts are required to test whether the therapeutic manipulation of IL-6 trans-signaling efficiently prevents pro-arrhythmic signatures (ion channel function, APD phenotypes, QT prolongation, and ventricular arrhythmia vulnerability) in diseased ventricular tissues/myocytes, thus counteracting (a) the lack of tissue specificity in current anti-cytokine treatments, (b) the redundancy of cytokines, and (c) the undesired side effects elicited by breaching the essential homeostatic role of classical IL-6 signaling.