In addition to overexpression of upstream receptor tyrosine kinases EGFR and ErbB2 that are well known to activate Ras pathway as part of the oncogenic signaling program [37, 38], recent evidence has identified other oncogenic events that can activate the Ras pathway in breast cancer, including recurrent mutations in MAP3K1 [17, 39, 40] and mutations of RASAL2, a RasGAP gene that functions as negative regulator of Ras [41]. This evidence concerns the gene MAP3K1 and breast cancer.