Given the “Moonlighting” function of cholesterol pathway enzymes and metabolites [2], we speculate that NSDHL knockdown may result in an accumulation of MAS, which influences EGFR degradation, and dysregulated EGFR-mediated signals suppresses SREBP1 expression, leading to the suppression of lipogenesis, cholesterol biosynthesis, and breast tumor growth and metastasis (Fig. 6b). The gene discussed is SREBF1; the disease is breast neoplasm.