We have previously demonstrated that sepsis selectively upregulates uncoupled eNOS, phosphorylated at the Thr-495 phosphorylation site in the renal medulla [24], suggesting that sepsis-induced renal microcirculatory dysfunction and AKI is partly driven by impaired nitric oxide bioavailability, In the present study, sodium ascorbate markedly increased phosphorylation of eNOS at the Ser-1177 residue, the activation site associated with proper enzyme coupling, which can enhance nitric oxide signalling and bioavailability. The gene discussed is NOS3; the disease is Sepsis.