Particularly, we investigated: i) the impact of CAFs and adipocytes isolated from stromal breast tissues on mammosphere formation and self-renewal in breast cancer cells; ii) the specific role of leptin and its receptor in influencing breast CSC phenotype in the context of the tumor microenvironment; iii) the effect of inhibiting leptin signaling as potential therapeutic target to reduce breast CSC activity in in vitro and ex vivo models. Here, LEP is linked to breast carcinoma.