Recently, GRK5 has been also described as a regulator of Lipopolysaccharide (LPS)- and Toll-like receptor (TLR)-induced inflammatory cytokine/chemokine production and immune cell tissue infiltration in vivo.9,13 Thus, the aim of the present study was to assess whether myocardial GRK5 levels can affect immune cell recruitment to the heart following MI and ultimately influence cardiac function and survival in a murine model of post-ischemic HF. This evidence concerns the gene GRK5 and myocardial infarction.