Moreover, it has been demonstrated that (1) silica12,18 and uric acid10,17 activate the inflammasome via P2X7 signaling, (2) treatment with a P2X7 inhibitor reduces IL-1ß release10,12,18, (3) oxalate crystal-induced ATP release contributes to kidney inflammation8 and (4) several studies have suggested that P2X7 may be a suitable pharmacological target in various renal diseases, such as diabetic nephropathy19,20, glomerulonephritis21, hypertension20, kidney injury induced by metabolic syndrome22 and ischemic acute kidney injury23. The gene discussed is P2RX7; the disease is medical procedure.