Thus, paradoxically, [L2Zn3]6+ causes dephosphorylation of T172 AMPKα and kinase inhibition in a cell-free system (Fig. 7a, g, h) and in the HCT116 cancer cells with brief exposure (Fig. 8b) consistent with its phosphatase activity (Fig. 4) but longer treatment results in increased cellular levels of T172P AMPK (Fig. 10) which is attributed to selective ATP depletion (Fig. 9b). The gene discussed is PRKAB1; the disease is cancer.