Since the expression levels of GRK2 protein in immune cells can vary during different disease states, including cardiac failure, rheumatoid arthritis, and multiple sclerosis, in both animal models and patients [36–42], and GRK stoichiometry can determine whether a GRK responds [42], the effect of this differential expression of GRK2 on physiological responses that leads to T-cell behaviors, such as CCR7-induced chemotaxis is important to define. The gene discussed is GRK2; the disease is heart failure.