First, we showed that Citral administration inhibited the increase in ROS and NO production and p47phox levels seen in FSGS mice and activated the Nrf2 signaling pathway involving increasing expression of its downstream molecules NQO1 and HO-1 during the early developmental stage of this FSGS model, thus contributing to the beneficial effects of Citral on the treated mice (Figure 3). This evidence concerns the gene HMOX1 and focal segmental glomerulosclerosis.