Because the two most common mechanisms regulating TGF-β1 signaling in the same cell are self-induced feedback loops (responsible for regulation of self-supported proliferation) and cross-talk with RTK-dependent pathways [51], we explored potential therapeutic effects of anti-Activin A, anti-Gremlin 1 and anti-TGF-β antibodies using two different scenarios, i.e., without additional exogenous stimuli and in the presence of PDGF-BB, which is up-regulated in PAH lungs, promotes PAVSMC proliferation, and activates Akt, p38 MAPK and ERK1/2 [6,26,52]. The gene discussed is GREM1; the disease is pulmonary arterial hypertension.