For the sake of simplicity, we considered the set of interactions reported for breast cancer cells during matrix-deprivation (Figure 2A): (a) AMPK and Akt can switch back and forth between their phosphorylated (active) and dephosphorylated (inactive) forms, (b) phosphorylated AMPK (pAMPK) can upregulate the levels of PHLPP2 which promote the dephosphorylation of Akt, and (c) phosphorylated Akt (pAkt) can upregulate the levels of PP2Cα associated with AMPK, thus enhancing AMPK dephosphorylation. The gene discussed is AKT1; the disease is breast carcinoma.