By contrast and despite AMPK-α1/α2 deletion occurring in all smooth muscles, histological assessment of the systemic vasculature in terminal samples with haematoxylin/eosin and α-smooth muscle actin revealed no evidence of hepatic centrilobular congestion or fibrosis, arteriolar hyalinosis or hypertrophy within the tunica media or intima of renal arteries from AMPK-α1/α2 knockouts (Fig. 3ei-ii), nor vasculopathy or any other evident lesion of the brain (Supplementary Fig. 9 and Supplementary Table 2). This evidence concerns the gene PRKAA1 and vascular disorder.