Although the physiological function of TRPC6 channels in the heart in normal conditions remains poorly understood, it has been reported that abnormal influx calcium through TRPC6 channels in response to different types of stress such as increased ROS, PLC and DAG activation, Excessive stimulation by endothelin1, angiotensin II, and vasoconstriction activates calcineurin and NFATs and leads to pathological hypertrophy and heart failure [13, 21]. The gene discussed is AGT; the disease is heart failure.