In consequence, if we can stop the release of the CCL-2, OPN, and ROS, inhibit the oxidative stress and inflammatory injury and apoptosis of renal tubular epithelial cells caused by crystal reaction, and learn more about the regulation mechanism of Fetuin-A, it will help us to understand more about the formation mechanism of Randall’s plaques, and may provide new ideas for further elaboration of the pathogenesis of urolithiasis. The gene discussed is SPP1; the disease is urolithiasis.