TNF plays a regulatory role in reducing, maintaining and improving inflammatory responses, and Riva C et al also explored auditory function in cd/1 mice at 4, 12, and 24 weeks of age and correlated it with the presence of oxidative damage in the cochlea and the regulation of cochlear HIF-1 responsive target genes, associated with multiple inflammatory pathways such as TNF-α, or cell death with p53 protein, Bax protein and surviving factors with insulin-like growth factor-1.[44] Furthermore, hypoxia modulates molecular processes in both acute and chronic tinnitus. This evidence concerns the gene BAX and Tinnitus.