An opposite finding performed by other researchers suggests that MNF2 can suppress PERK activity through direct interaction under basal conditions, but hyperglycemia inhibits MFN2 expression and promotes the reduction of MNF2-PERK interaction, thereby MNF2 overexpression could alleviate the abnormal activation of PERK pathway, cardiomyocytes apoptosis and mitochondrial dysfunction (139, 140). The gene discussed is EIF2AK3; the disease is Hyperglycemia.