Taken together, it is conceivable that Wnt5a-ROR1/STAT3 signaling in OC samples reflects a phenotype associated with pro-inflammatory traits for both epithelial ovarian cancer and stromal cells through a feedback loop that involves a STAT3-mediated upregulation of Wnt5a/ROR1 signaling, which in turn could initiate STAT3 signaling via pro-inflammatory pathways (Suppl. Here, WNT5A is linked to ovarian carcinoma.