When compared with control subjects, a greater increase in AMPK activity was observed in HSVECs from patients with CAD and T2D (0.062±0.011 compared with 0.022±0.006 nmol·min−1·mg−1; P=0.01; Figure 3A) than in cells from patients with CAD alone (0.031±0.005 compared with 0.022±0.006 nmol·min−1·mg−1; P=0.26; Figure 3A). Here, PRKAA1 is linked to coronary artery disorder.