The expression of GLUT2 in pancreatic β cells could also be associated with the level of lncRNA-p3134 in circulation.[23]A previous study on Wiskott–Aldrich syndrome showed that endosomal WASH protein deficiency could influence the transport of GLUT2 protein in pancreatic β cells, consequently reducing the intracellular GLUT2 level and synthesis of protein, in turn, inducing the elevation of blood glucose [24]. This evidence concerns the gene SLC2A2 and hereditary thrombophilia due to congenital protein S deficiency.