Sialoglycan dysregulation resulting from disrupted glycan synthesis can be attributed to the following two primary pathways: the emergence of sialic acid-modified truncated O-glycans, which reveals the tumor-associated carbohydrate antigen sTn [28] and is linked to ST6GALNAC1 upregulation and C1GALT1C1 alterations [29,30], and augmented sialic acid residues on the cancer cell surfaces, which is attributed to aberrant sialyltransferase and neuraminidase activities [31]. The gene discussed is ST6GALNAC1; the disease is neoplasm.