Indeed, all these processes are coordinated by copper-dependent enzymes: (i) the lysyl oxidase family (LOXs and LOXLs), which promotes ECM cross-linking and stiffness; (ii) the phosphatidylinositol 3-kinase (PI3K)/RAC-alpha serine/threonine-protein kinase (AKT) pathway, whose dysregulation is associated with cancer cell survival, the EMT, and resistance to apoptosis; and (iii) the mitogen-activated protein kinase MEK1/2 which, in turn, phosphorylates extracellular signal-regulated kinase 1/2 (ERK1/2), driving cancer cells through proliferation and EMTs [19]. The gene discussed is AKT1; the disease is cancer.