We did not assess the mechanisms by which arrhythmia inducibility was reduced in TRPV4−/− mice compared to TRPV4+/+ mice, which could be explained by mere reduction in the arrhythmogenic substrate (i.e., fibrosis) or by specific antiarrhythmic mechanisms as opposed to CM, as suggested by recent reports [38]. This evidence concerns the gene TRPV4 and cardiac arrhythmia.