Obesity is identified as a casual factor in both the development as well as the progression of breast carcinogenesis (3, 4), and is characterized by rapid adipose tissue remodeling (hypertrophy and hyperplasia) (5), increased synthesis of several adipokines such as leptin, resistin, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, macrophage chemoattractant protein-1 (MCP-1), and immune cell infiltration, all of which lead to a state of sustained low-grade inflammation. This evidence concerns the gene RETN and obesity disorder.