We used our SIRT1-deficient mouse model to verify a regulation of glycolysis proteins by SIRT1 in pancreatic lesions in vivo. When comparing immunostainings in the PanIN lesions in KC;Sirt1-lox versus KC controls, we found a weaker staining for GLUT1 (Glucose transporter 1), GAPDH (Glyceraldehyde 3-phosphate dehydrogenase) and PKM2 (Pyruvate kinase isozyme m2) and slightly weaker HK2 (Hexokinase 2) (Figure 2). The gene discussed is GAPDH; the disease is keratoconus.