Our findings indicate that being part of ERβ signaling is an important mechanism for ZFHX3’s tumor suppressor activity in prostate cancer, as ZFHX3 is clearly upregulated by activated ERβ in C4-2B cells (Fig. 1), and repression of MYC transcription by ERβ required the interaction of ERβ with ZFHX3 (Figs. 4 and 5). This evidence concerns the gene ESR2 and prostate carcinoma.