To investigate the role of PAR1 signaling in breast tumor growth and vascularization in vivo, we over-expressed wt hPar1 and deletion constructs [e.g., L369Z, which lacks the entire cytoplasmic tail, and Y397Z, which exhibits persistent signaling due to impaired internalization [11], [12]] in MCF7 cells. This evidence concerns the gene MARK2 and breast neoplasm.