Our findings are in agreement with previous reports where gliflozins were able to inhibit the PERK-CHOP pathway of UPR acting on PERK activation itself, as shown in the brain of rat model of Parkinson's disease [28], in the heart of I/R injury mouse model [62] and in doxorubicin induced cardiac fibrosis and apoptosis in Streptozotocin (STZ) rats [63]. This evidence concerns the gene EIF2AK3 and Parkinson disease.