Given this finding, together with the observation that TRPV4, eNOS and caveolin-1 are preferentially co-localized and functionally interactive in the caveolae of certain vascular endothelial cells (Sowa, 2012; Goedicke-Fritz et al., 2015), it is possible to hypothesize that a decrease in the number of endothelial caveolae is causally connected to the downregulation of endothelial TRPV4 expression and thus to the endothelial dysfunction in diabetes. This evidence concerns the gene CAV1 and endothelial dysfunction.