A previous study, which demonstrates that the decrease in Sestrin 2 expression and consequent mTOR activation in PECs is strongly associated with the development of glomerular hyperplastic-like lesions and periglomerular fibrosis in animal models of puromycin nephropathy and crescentic glomerulonephritis, supports the idea that Sestrin 2 has a critical role in regulating the PEC phenotype [31]. The gene discussed is SESN2; the disease is crescentic glomerulonephritis.