For example, the activation of the mTOR pathway has been shown to occur in both human and mouse lupus nephritis [33], and anti-Thy1.1-induced chronic glomerulosclerosis in the rat [34], [35], but these nephritic lesions were associated with a reduction in protein synthesis due to the activation of protein kinase R (PKR)-like ER kinases (PERK) and phosphorylation of eIF2, as a compensatory mechanism [36]–[38]. This evidence concerns the gene EIF2AK3 and lupus nephritis.