Simulating glucose transporter expression in a β-cell from a T2D donor, by inhibiting HNF1A and FOXA2 translocation to the nucleus, without further modifications, we calculated that in disease conditions 92% of the glucose transporters present at the β-cell surface are GLUT-1 and 8% are GLUT-2. Here, HNF1A is linked to type 2 diabetes mellitus.