These lines of reasoning included: (a) cell metabolic specificity related to the Warburg effect, overproduction of lactate and carbonic acids, and an alteration of membrane transport as a result of intracellular pH (pHi) regulation; (b) an unusually high number of proteins implicated in the transport of chloride; (c) metabolic alterations resulting from SLC6A8 overexpression and a possibility of increased uptake of creatine phosphate; (d) a loss of integrin dependent adhesion and AML cell mis-homing triggered by a massive modification of the ion transport within the niche microenvironment. The gene discussed is SLC6A8; the disease is acute myeloid leukemia.