ACADM, a medium‐chain acyl‐CoA dehydrogenase, initiated β‐oxidation, an aerobic process by which fatty acids are degraded into acetyl‐CoA for energy production.[22] ACADM has been identified as a tumor suppressor that inhibits tumorigenesis and tumor progression in liver and pancreatic cancers.[23] Our study demonstrated that N‐glycosylation modification at the residue 263 of CTSD modulated the expression levels of ACADM and ferroptosis‐related proteins, including ACSL4, SLC7A11, and GPX4, thereby altering the biological behaviors of CRC cells. Here, CTSD is linked to neoplasm.