The U-STAT3 to support the expression of many genes in response to angiotensin II depends upon the acetylation of Lys685,[90] consistent with a previous study[67,91] that activation of the AT1R leads to nuclear accumulation of U-STAT3 and promotes its interaction with the acetyl transferase p300, inducing the expression of proteins involved in cardiac hypertrophy and dysfunction. Here, AGTR1 is linked to cardiac hypertrophy.