In addition, prior work demonstrates that CAF programs—such as MFAP5‐FAK–ERK signaling that modulates vascular permeability and drug delivery, and WNT5A‐driven niche support for ovarian cancer stemness—are tractable in stromal–epithelial models, reinforcing the value of stable stromal lines for mechanistic and translational studies [2, 11]. Here, MFAP5 is linked to ovarian carcinoma.