Although as discussed above it is clear that enhanced activity of GRK2 in HF negatively affect βAR signaling, we have recently demonstrated that GRK2 can induce myocardial pathology through other systems including non-GPCR activity that can negatively affect myocyte metabolism and cell survival (Brinks et al., 2010; Ciccarelli et al., 2011; Chen et al., 2013; Fan et al., 2013). This evidence concerns the gene GRK2 and hydrops fetalis.