This expectation is consistent with a previous study showing that haploinsufficiency of AIB3 (NCOA6), a coactivator required for PPAR and RXR transcriptional activity, accelerated mammary tumor development in MMTV-polyoma middle T antigen mouse model and the AIB3+/- tumors also were less sensitive to the inhibitory effects of PPARγ and RXR ligands [52]. This evidence concerns the gene PPARA and breast cancer.