In contrast, in the same model, adding ERβ to the cells prevented tumor formation by estrogen stimulation via inhibiting the expression of transcription factors (e.g., c-myc, cyclin D1, cyclin A) and increasing the expression of P21 and P27 (causing cell cycle arrest), indicating the antagonistic effects of ERβ against ERα [16,17]. The gene discussed is ESR2; the disease is neoplasm.