SMAD2 and polycystic ovary syndrome: Spatial transcriptomics revealed enhanced co-localization of these molecules within Lrp2high TCs in PCOS ovaries, underscoring their role in abnormal cellular proliferation and supporting prior evidence linking dysregulated TGF-β signaling to PCOS pathophysiology (Wang and Li, 2023; Wang S. et al., 2022) Functional studies further demonstrated that knockdown of Inhba, Smad2 or E2f4 significantly reduced DHEA-induced TCs proliferation, with the most pronounced effect observed upon Inhba silencing.