In our previous study, we believe that IH is the most powerful incitant involved in OSAH-induced cardiac remodeling, and we conclude that IH-induced cardiac microvascular fibrosis is associated with Endothelial-to-Mesenchymal Transition (EndMT) and inhibiting HIF-1α could improve EndMT5, However, the etiology and lesion location of OSAHS are complex, and no one-size-fits-all treatment is available for it6. Here, HIF1A is linked to isolated hemihyperplasia.