Considering that analysis of RA target genes revealed overexpression of Cyp26a1 (Fig. 7B), which is indicative of enhanced RA signaling, we investigated the possibility that the enhanced hepatic RA signaling in T1D might be due, at least in part, to the changes in expression and/or subcellular localization of RDH10 caused by metabolic stress and metabolic remodeling associated with T1D. This evidence concerns the gene CYP26A1 and type 1 diabetes mellitus.