In breast cancer, depletion of UTX resulted in upregulation of Myc-dependent expression of EMT factors, including SNAI and ZEB1/2.315 Thus, by forming a transcriptional repressive complex with LSD1, HDAC1 and DNMT1, UTX is a tumor suppressor and a negative regulator of EMT-induced CSC-like properties in breast cancer.314 However, pro-tumor functions of UTX were observed in the ER + subtype of breast cancer cells where the transactivation of UTX and estrogen receptor (ER) forms a feed-forward loop in response to hormone treatments.316. Here, MYC is linked to neoplasm.