In addition, increased GRK2 levels in cardiac fibroblasts contribute to enhanced collagen synthesis and fibrosis and appear to favor maladaptive remodeling upon ischemia/reperfusion injury (Woodall et al., 2016), whereas inhibition of the Gβγ-GRK2 axis limits pathological myofibroblast activation after myocardial ischemia (Travers et al., 2017). This evidence concerns the gene GRK2 and ischemia.