However, results from large-scale association studies and functional experiments support the increased role of the skin barrier in the disease predisposition and, thus, the underlying genetic variability [19]; variants mapped to the desmoglein family (e.g., DSG1 and DSG3) [20,21], corneodesmosin (CDSN) [22], and the protease inhibitor SPINK5 represent the epidermal barrier dysfunction as the primary pathogenetic event during eczema pathogenesis [23]. This evidence concerns the gene SPINK5 and Eczematoid dermatitis.