SMAD2 and cancer: INHBA+ (Activin A–producing) cancer-associated fibroblasts upregulate PD-L1 via SMAD2-dependent signaling and drive regulatory T-cell differentiation; neutralization of Activin A attenuates disease and remodels the immune–stromal compartment in ovarian models, indicating a rational partner for PD-(L)1 or costimulatory strategies in INHBA-high states (96–98).