In light of data reporting the downregulation of β2-chimaerin in breast cancer [20], and based on mechanistic insights showing that β2-chimaerin and Rac1 regulate cell proliferation, migration and invasion downstream of ErbB receptors [24, 33, 34], we selected the MMTV-Neu mouse model, which develops breast cancer due to overexpression of the Neu (ErbB2/Her2) receptor, to study the effects of β2-chimaerin deficiency in vivo. This evidence concerns the gene RAC1 and breast carcinoma.