The genetical depletion of TLR2, TLR4, and especially MyD88 in CLP-induced sepsis resulted in reduced neutrophils infiltration into the kidney, decreased expression of proinflammatory cytokines, iNOS, MPO and a significant improvement in kidney function, indicating that neutrophils participate in polymicrobial SAKI mainly through the MyD88 pathway [100]. The gene discussed is TLR4; the disease is Sepsis.