In AIS, the neuroinflammatory response is closely related to neuronal apoptosis, and NF-κB signaling mediated by TLR2 and TLR4 through the MyD88-dependent pathway can activate apoptosis [19] in response to changes in the expression of proapoptotic markers (e.g., Bax, Caspase3) and the anti-apoptotic protein Bcl-2 [20]. Here, TLR4 is linked to androgen insensitivity syndrome.