In the in vitro model of corneal dystrophy, the effects MSC-EVs were compared with those of SER-EVs. SER-EVs exhibited minimal or absent effect on modulating endoplasmic reticulum stress and/or apoptosis. MSC-EVs caused downregulation of genes causing endoplasmic reticulum stress in an endoplasmic reticulum stress model in HCECs. MSC-EVs upregulated the Akt pathway, while also decreasing activation of apoptotic markers. The therapeutic effects of MSC-EVs is likely linked to the transfer of endoplasmic reticulum-stress targeting miRNAs to corneal endothelial cells. This evidence concerns the gene AKT1 and corneal dystrophy.