In our current study, in matrix-deprived MDA-MB-231 breast cancer cells, we observed the activation of AMPK via phosphorylation of Thr172 residue and also functionally by the phosphorylation of its bona fide substrate ACC (Acetyl-CoA carboxylase) at Ser79 residue (Supplementary Figure S1A). The gene discussed is PRKAA1; the disease is breast cancer.