The agonist‐dependent phosphorylation of the AT1R is substantially increased in human embryonic kidney cells overexpressing GRK5, GRK2, or GRK3.97 GRK4 and GRK5 impair both the sensitivity and maximum response of D1R, whereas GRK2 and GRK3 impair only the sensitivity of D1R to agonist stimulation.16, 98 Whereas HDAC1 is involved in the increase in GRK4γ142A>V‐mediated increase in renal AT1R expression,77 HDAC5 is associated with the GRK5‐regulated gene transcription in heart failure.99 This evidence concerns the gene GRK3 and heart failure.