XYT has been shown to reduce heart failure in animal models[18,25–30] by lowering serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), endothelin-1 (ET-1), angiotensin II (Ang II), aldosterone (ALD), improving cardiac ultrastructure, intervention of (Akt/AMPK)-mTOR signaling pathway, down-regulation of autophagy, reducing myocardial apoptosis, increasing left ventricular ejection fraction and shortening rate, delaying ventricular remodeling, inhibiting myocardial fibrosis, and improving cardiac function. Here, MTOR is linked to heart failure.