It is suggested that, being a cation, metformin could accumulate in the mitochondria at 100-500 times higher concentrations due to the mitochondria membrane potential, leading to an effective inhibition of complex I. Overall, metformin should be able to mediate AMPK activation and anti-tumor activity, in human tumors with serum levels that are clinically achievable with standard anti-diabetic doses of the drug, indicating that metformin doses used in current clinical trials are appropriate. Here, PRKAA1 is linked to neoplasm.