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. This evidence concerns the gene P2RX7 and urogenital neoplasm.