To evaluate the impact of EDA + FN alternative splicing on endothelial function during diabetes, we used male mice from two engineered mouse strains26 lacking regulated splicing of fibronectin EDA exon, one constitutively including (EDA+/+) and the other constitutively excluding the exon (EDA−/−), due to the optimization of the EDA splicing sites and to the targeted deletion of the EDA exon, respectively. This evidence concerns the gene FN1 and diabetes mellitus.