Thus, the reduction in N-[11C]methyl-AMD3465 uptake in the tumor after treatment with AMD3100 observed in this study is likely the result of a combination of saturation of the CXCR4 receptors by the antagonist and a reduction in T-cell infiltration by inhibition of CXCR4-mediated chemotaxis. Here, CXCR4 is linked to neoplasm.