Our data showed that overexpression of FOXP2 activated oncogenic MET signaling in FOXP2-transformed prostate epithelial cells and human prostate tumors, and inhibition of MET signaing activation in FOXP2-overexpressing RWPE-1 cells and NIH3T3 cells significantly suppressed the anchorage-independent growth or foci formation of these cells. This evidence concerns the gene FOXP2 and prostate neoplasm.