PELI1 and atopic eczema: Although the treatment of mouse skin with DNCB increased the thickness of the epidermis and recruitment of immune cells to the dermis along with production of secretory Periostin, a matricellular protein known to contribute to clinical features of atopic dermatitis28,29, we failed to detect the induction of Peli1 in atopic dermatitis-like inflammation (Fig. 1d).