We found that the alternative splice isoform expressed in basal subtype breast cancer cells functions very differently from the previously identified functions of the isoform found in normal mammary epithelial cells and in luminal subtype breast cancer cells, and moreover that depletion of the ARHGEF11 isoform expressed in invasive breast cancer cells suppressed their malignant phenotype both in vitro and in vivo. This evidence concerns the gene ARHGEF11 and invasive breast carcinoma.