Cardiac function vastly depends on the composition and structure of the ECM. Fibrillar collagen in the ECM generates a complex meshwork to support the cardiac cells by providing structural and biochemical support. Therefore, cardiac function is largely affected by any disturbance of the ECM to contribute to the progression of cardiac diseases. Along these lines, LOX overexpression induced cardiac hypertrophy and dysfunction, triggering fibrotic response that is characterized by stronger collagen deposition and cross-linking and high expression of fibrotic markers¹ . Lysyl oxidase inhibition was shown to reduce the fibrotic mediators, such as collagen crosslinking, and ameliorated the cardiac dysfunction^2,3.