Binding of AMP or ADP to a crucial site on the AMPK γ subunit (where they displace ATP) then activates AMPK by a complex mechanism (discussed in Section 2) involving phosphorylation at a conserved threonine residue on the α subunit (Thr172) by the upstream kinase and tumour suppressor, LKB1. This evidence concerns the gene PRKAB1 and neoplasm.