The precise reason why thedisruption of EDA-A2/XEDAR interaction does not lead tothe ectodermal dysplasia phenotype is currently unknown andrequires further investigation, however, studies have shownthat EDA-A2 is expressed primarily in aging adipose tissue,arteries, heart, lungs, muscle, and skin, and may also regulateglucose metabolism, and serves as a predictor of steatosisaggravation in patients with non-alcoholic fatty liver disease(Yang et al., 2015; Cai et al., 2021). Here, EDA is linked to ectodermal dysplasia syndrome.