Additional studies of the mammary gland after lactation have revealed that these phenotypes are driven, in part, by mammary and tumor specific increases in pro-inflammatory cyclooxygenase-2 (COX-2), fibrillar collagen, semaphorin 7a (SEMA7A), bone marrow derived stromal and macrophage populations, lymphangiogenesis, and circulating estrogens[15–22]. This evidence concerns the gene SEMA7A and neoplasm.