We also demonstrated that the luminal B subtype was remarkable in tumors overexpressed ROCK, suggesting that high expression level of ROCK may be affected by HER2 expression of breast tumors. Exposure to physiological concentrations of 17β-estradiol in human umbilical vein endothelial cells resulted in the interaction between ERα and Gα13 (heterotrimeric G protein) to induce RhoA/ROCK activity [83]. This evidence concerns the gene ERBB2 and breast neoplasm.