The use of a second model, the NEP25 mouse model [14], was prompted by our interest to further assess the role of DDR1 in a injury model where PEC-induced glomerulosclerosis is caused by podocyte depletion in absence of intra-glomerular inflammation, primary mesangiolysis and primary hypertension thus further strengthening the role of DDR1i in the protection of glomerular function also in a model of focal segmental glomerulosclerosis. This evidence concerns the gene DDR1 and focal segmental glomerulosclerosis.