For example, the accumulation of TMAO levels in the body promotes renal fibrosis, inflammation, and atherosclerosis, thereby accelerating the progression of CKD (166, 167); high betaine levels may lead to abnormal methylation of profibrotic genes (such as TGF-β and COL1A1), promoting renal interstitial fibrosis (168); and methylation cycle disorders in patients with CKD lead to homocysteine accumulation, whereas abnormal betaine metabolism may exacerbate reactive oxygen species production, promoting renal tubular damage (169). The gene discussed is TGFB1; the disease is chronic kidney disease.