Cytoplasmic SHMT1 directs the allocation of folate‐activated one‐carbon units toward thymidylate or SAM biosynthesis.[55] Since SAM is the major cellular methyl donor, dysfunction in this SHMT1‐driven pathway impairs cellular methylation and genome stability, thereby providing a mechanistic basis for elucidating the distinct contributions of these metabolic pathways to CRC risk.[55] We demonstrated that SHMT1 played a crucial role in CRLM by regulating formate production, thereby modulating cellular energy metabolism, as evidenced by inhibited AMPK activity. Here, SHMT1 is linked to colorectal carcinoma.