The critical inflammatory mediators that are up-regulated in obesity-associated BC perpetuate the carcinogenic process and exhibit redundant effects by stimulating multiple and overlapping signaling pathways that converge to stimulate aromatase expression/activation, resulting in aberrant local estrogen production, which promotes cell proliferation and/or inhibits apoptosis, and stimulate the production of additional inflammatory mediators within mammary tissue, ultimately resulting in tumorigenesis. This evidence concerns the gene CYP19A1 and Obesity.