MLST8 and Hyperglycemia: According to our data, we summarized the underlying mechanism how does maternal high glucose condition affect fetal lung development (Fig. 6): maternal hyperglycemia shifts dynamic assembly of mTORC1 and mTORC2 toward mTORC1 assembly by upregulating TRAF2-mediated GβL ubiquitination, which inhibits mouse fetal lung angiogenesis, thus affecting fetal lung health.