Next, we assessed the specific mTOR inhibitor rapamycin or silenced TAZ with siRNA to clarify whether the enhancement of breast cancer stemness induced by overexpressing TMEM120B was dependent on the activation of both signaling pathways.Western blotting results revealed that adding 2 nmol rapamycin for 48 h or inhibiting TAZ may counteract the increase in the proliferation, invasion, and stemness of SK-BR-3 cells induced by TMEM120B overexpression (Additional file 3: Fig. S4B-G). The gene discussed is MTOR; the disease is breast carcinoma.