Figure 1A shows that metformin treatment significantly increased AMPK activation, as measured by phosphorylation of AMPK on residue Thr172, in both control (P<0.01) and CFS (P<0.05) myotubes, compared with untreated. Compound 991 treatment had a similar effect, significantly increasing AMPK activation over untreated myotubes in both control and CFS (P<0.05, both) (Figure 1B). This evidence concerns the gene PRKAA1 and myalgic encephalomeyelitis/chronic fatigue syndrome.