Three approaches have been taken to optimize recruitment the SDF-1-CXR4 axis in the setting of ischaemic heart disease: (a) supplying artificial SDF-1α to match peak CXCR4 expression; (b) augmenting CXCR4 expression to meet the period of maximal SDF-1α release; and (c) minimizing SDF-1α degradation by dipeptidyl peptidase 4 (DPP4) and other proteases. The gene discussed is CXCL12; the disease is heart disorder.