Furthermore, in this study, we observed that TRPC3 knockdown was associated with increased expression of (i) SREBP-1c, which controls hepatic de novo lipogenesis; (ii) DGAT2, which controls TG synthesis; and (iii) VLDLR, which controls lipid uptake; and with decreased expression of (i) CPT1α, which controls FFA β-oxidation; (ii) ATGL (adipose triglyceride lipase), which catalyzes the hydrolysis of TGs in AF mouse liver (Fig. 4d and e). The gene discussed is VLDLR; the disease is atrial fibrillation.