Conversely, in cancers like KIRC and STAD, where other oncogenic pathways might be more dominant or where a higher degree of differentiation is maintained, high DSN1 expression could reflect a less aggressive subtype or distinct underlying biology where excessive DSN1 triggers immunogenicity (via elevated TMB/MSI) and mitotic catastrophe (through unresolved chromosome missegregation), tipping the balance toward tumor suppression 44. Here, DSN1 is linked to neoplasm.