Furthermore, intracellular overexpression of PCSK9 results in decreased FFA uptake and utilization through a specific mechanism: PCSK9 competes with FFAs for binding to the CD36/FAT receptor and reduces their membrane recycling, resulting in an increase in systemic FFA levels and a significant reduction in fatty acid beta oxidation and the Krebs cycle [67]; this is the primary driver of atherosclerosis and cardiomyocyte injury processes. The gene discussed is CD36; the disease is atherosclerosis.