Transmembrane protein 79 (TMEM79, a predisposition gene for AD) can specifically inhibit ubiquitin-specific peptidase 8 deubiquitination, and its deficiency shows more susceptible to developing skin inflammation, compromised barrier function, and spontaneous dermatitis (Lim et al., 2013; Sasaki et al., 2013; Saunders et al., 2013; Chen et al., 2020). This evidence concerns the gene TMEM79 and dermatitis.