These findings corroborate the similar enrichment of SS18-SSX targets in both the breast and pancreatic ColX modules (Fig. 2E), suggesting that common pathways involving dysregulated cell proliferation and tissue remodeling are involved in both cancer and OA (Table S5A), as well as the differential activation of NUP214 targets in high-ColX module breast and male pancreatic tumor samples (Fig. 3C), which additionally suggest a shared pathogenic mechanism linked to aberrant transcription regulation (Table S5B). This evidence concerns the gene NUP214 and pancreatic neoplasm.