Indeed, a very recent study shows that ALK1-overexpression could normalize SMAD and NOTCH target gene expression, restore the effect of BMP9 on suppression of p-Akt, and inhibit the development of AVMs in Alk1- and Eng-inducible knockout mice, suggesting that ALK1 overexpression or activation might be a potential therapeutic strategy for HHT patients (Kim et al., 2020). Here, GDF2 is linked to hereditary hemorrhagic telangiectasia.