Leptin is the product of the ob gene that plays a pivotal role in regulating food intake, energy expenditure and neuroendocrine function; furthermore, high levels of leptin have been frequently observed in obese subjects [6, 7, 8]. Several published studies have shown that leptin can regulate endothelial cell proliferation and promote angiogenesis; moreover, it has an association with progression and poor survival of BC [9, 10, 11]. Leptin exerts it physiological action through the leptin receptor which is overexpressed in BC . Genetic variations in some obesity-related genes have been demonstrated to affect BC risk by the levels and functioning of leptin [13, 14, 15]. Over the past few decades, two obesity-related gene polymorphisms have been most commonly reported: LEP G2548A rs7799039, and LEPR Q223R rs1137101. Leptin G2548A polymorphism, located in the promoter region of the leptin gene, has been demonstrated to correlate with variations in serum leptin levels, degree of obesity, as well as cancer susceptibility [16, 17]. LEPR Q223R polymorphism alters amino acid change from neutral to positive that could affect the functionality of the receptor and modifies its signaling capacity [18, 19].