MDK and neoplasm: Conversely, CD99–CD99 interactions were upregulated in both incoming and outgoing directions, consistent with tumor-suppressive roles of CD99 [44], while MDK–NCL and MDK–ITGA6_ITGB1 interactions, typically linked to CAF activation and cancer cell adhesion [45,46], were also elevated in PIAS1+ CAFs; these may have context-dependent functions in OSCC.