In one of them, Wang et al [27], using human fibroblasts as a replicative senescence model, found that incubation with various AMPK activators, including AICAR for 3–7 days triggered senescence characteristics, such as the acquisition of SA-Gal activity and increased p16INK4a expression, whereas infection with a DN-AMPK decreased SA-Gal activity. The gene discussed is PRKAA1; the disease is infection.