Like the others, we did not detect the changes of BMPR2 and its downstream signaling component phopsho-Smad1/5/8 in the whole-lung lysates of rats of SuHOX model45, however Axl inhibition triggered the decline of BMPR2 signaling both on the level of BMPR2 and phospho-Smad1/5/8 proteins, as well as EC-specific downstream target of BMPR2, E-selectin, confirming the detrimental impact of Axl inhibition in the context of PAH. The gene discussed is SMAD1; the disease is pulmonary arterial hypertension.