These results, in combination with the inhibitory effects that FOXP1 knock down has on breast cancer cell growth both in vitro and in xenografts, imply that some of the tumor promoting properties of PRMT5 are mediated through FOXP1, and further suggest that PRMT5 inhibition might be a viable therapeutic option that should be explored in breast cancer treatment. This evidence concerns the gene FOXP1 and neoplasm.