In addition, ARNT1 has been shown to be a potent coactivator of ERs, because their LBDs interact after E2 activation with the c-terminal transactivation domain (TAD) of ARNT1 [43], but this seems to be cell line specific, since Labrecque and colleagues showed that, in contrast to MCF7 cells, ARNT exhibited a dioxin-independent co-repressor function for estrogen signaling in human ECC-1 endometrial carcinoma cells [44]. The gene discussed is ARNT; the disease is endometrial carcinoma.