ILK and polyarteritis nodosa: Both integrin α3β1 and ILK are key molecules in podocyte detachment, ILK is in its inactive state under normal resting conditions, PAN-induced podocyte damage could activate ILK, and active ILK can phosphorylate the cytoplasmic domain of β1-integrin, which results in a low-affinity binding state and podocytes are detached from the GBM[15-18].