Building on the work of Hatano et al., Adapala et al. utilized novel pharmacologic tools to determine how TGFß1-induced TRPV4 activation and the subsequently increased intracellular Ca2+ flux affects cardiac fibroblast activation and differentiation into myofibroblasts, the cellular entities primarily responsible for ECM deposition, and remodeling following myocardial infarction (Biernacka and Frangogiannis, 2011; Adapala et al., 2013). This evidence concerns the gene TRPV4 and myocardial infarction.