Further use of orthotopic transplant models of RON-overexpressing murine breast cancer cells with and without HGFL knockout into HGFL+/+ and HGFL−/− hosts further bolstered that HGFL overexpression in mammary tumors is largely supportive of these phenotypes and plays significant roles in altering the tumor cell and macrophage secretome in a pro-tumor manner [3]. This evidence concerns the gene MST1 and neoplasm.