Mechanistically, the NF-κB–TGF-β1–YAP1 axis has been implicated in both the establishment and homeostatic maintenance of the myCAF state; co-inhibition of TGF-β1 and YAP1 partially reverses myCAF activation and increases tumor-cell sensitivity to enzalutamide (ENZ) [53]. The gene discussed is NFKB1; the disease is neoplasm.