It is well established that proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and IL-6, contribute to the development of AKI in septic patients [7–9], and the inhibition of proinflammatory cytokines was able to attenuate sepsis-associated AKI and improves survival outcome [10, 11]. This evidence concerns the gene IL6 and acute kidney injury.