The dysregulation of these pathways, whether due to genetic mutations (e.g., in methylenetetrahydrofolate reductase (MTHFR) or CBS) or deficiencies in cofactors (e.g., vitamins B6, B12, or folate), can lead to homocysteine accumulation and the development of hyperhomocysteinemia [4,5]. Here, MTHFR is linked to hyperhomocysteinemia.