With the continuous development of society and the progress of technology, especially the improvement in the field of medicine, the knowledge about BC is constantly updating as time goes on. Recently, obesity has been considered as one of the related factors for BC risk [3, 4]. However, the exact pathogenesis of obesity about this malignancy is still the world's unsolved mystery. Previous published studies have demonstrated that leptin, an adipocyte-derived satiety hormone, is associated with the proliferation, angiogenesis, progression, and poor survival in BC cells, especially in higher grade tumors [5, 7, 9]. Two obesity-related gene polymorphisms (rs7799039, and rs1137101) have been recognized as contributors to BC risk through regulating the level and activity of leptin. Leptin G2548A polymorphism in the promoter region of the leptin gene is a potential source of polymorphism affecting gene expression [16, 17]. LEPR Q223R polymorphism occurs in a region which encodes the extracellular domain of the leptin receptor, acts the function of the receptor, and impairs the ability of leptin to bind to its receptor [18, 19]. To date, the association between rs7799039 and rs1137101 polymorphisms and BC susceptibility remains inconclusive. Therefore, in the cause of a more precise evaluation, we performed this meta-analysis.