To show that ATF3 was directly involved, we knocked down the expression of ATF3 in human MDA-MB-157 cells and demonstrated that reduced ATF3 expression upregulated MIR145 and MIR143 expression, which led to downregulation of KLF4, SOX2, OCT4, MYC, and KRAS. Taken together, these results are consistent with a model in which ATF3 overexpression in the ATF3 mouse mammary tumors suppresses Mir145 and Mir143 expression, which, in turn, activates mammary cancer stem cells or stem cell-like cells to self-renew and turns on the expression of pluripotency genes [39]. This evidence concerns the gene SOX2 and breast cancer.