To begin to investigate whether specific mutations within this axis contribute to distinct epithelial morphogenic changes and nonautonomous vascular effects, we modeled two of the most common patient-derived breast cancer somatic genetic alterations from this pathway in isogenic, nontumorigenic MCF10A cells: ErbB2 receptor amplification (ErbB2amp, by wild-type HER2/ERBB2 overexpression) or a PI3Kα mutation (PI3KαH1047R, by PIK3CA(H1047R) expression) that renders PI3Kα constitutively active (Fig. 3a, b). This evidence concerns the gene PIK3CA and breast cancer.