Mechanistically, ST8SIA1 overexpression inhibited Janus kinase 2 (JAK2) and signal transducer and activator of transcription (STAT3) phosphorylation, leading to a significant decrease in downstream effectors involved in tumor progression, including matrix metalloproteinase-2 (MMP2), proliferating cell nuclear antigen (PCNA), cyclin D1, and B-cell lymphoma 2 (BCL2) [42]. Here, JAK2 is linked to neoplasm.