Preceding reports have shown that UA impaired Nitric oxide (NO) generation and induced endothelial dysfunction and smooth muscle cell proliferation [46, 47] In experimental and in vitro systems, UA appears to have the ability to induce inflammatory mediators, such as tumor necrosis factor α, [48] and potentially stimulates mitogen-activated protein kinase which are known to induce cardiac hypertrophy [49, 50]. The gene discussed is WNK2; the disease is cardiac hypertrophy.