Identification of p18 as a downstream target of Gata3 in restraining mammary epithelial cell proliferation prompted us to hypothesize that p18 deficiency may rescue mammary growth defects caused by Gata3 deletion, allowing us to investigate the role of Gata3 loss-of-function in controlling cell fate during mammary tumor development and progression. This evidence concerns the gene CDKN2C and breast cancer.