In related research reports, SLC31A1 also increases intracellular ROS levels by inhibiting hypoxia induction factor 1 expression and the NrF2-dependent ROS clearance system, enhances mitochondrial oxidative phosphorylation, and induces ROS accumulation.[34] In response to severe oxidative stress, NFE2L2 induces the expression of Klf9, which inhibits ROS suppressor enzymes and promotes cell death.[35] However, research on the mechanisms underlying the association between SLC31A1 and CES is lacking. This evidence concerns the gene KLF9 and cat-eye syndrome.