Overexpression of CRYAB in human mammary epithelial cells also formed invasive mammary carcinomas in nude mice, induced epidermal growth factor and anchorage independent growth, increased cell migration and invasion, and activated the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway, suggesting that CRYAB could be considered an oncoprotein [14]. The gene discussed is CRYAB; the disease is breast carcinoma.