TGFBR1 and neoplasm: Transforming growth factor-β1/β2/β3 from tumor cells, CAFs and Tregs drive exclusion via TGFBR1/ALK5-SMAD2/3 plus non-SMAD (p38/ERK/PI3K) arms, while CAF-derived Activin A (INHBA) engages ACVR1B/ACVR2 to phenocopy these suppressive effects and blunt PD-(L)1 responses (8–11).