For example, the overexpression of Cas activates growth and survival signaling pathways via phosphoinositide 3-kinase/Akt, ERK1/2, epidermal growth factor receptor, Rac, or Src, conferring doxorubicin or tamoxifen resistance [11]; activation and aberrant expression of Cas correlates with tumor progression and metastasis; and overexpression is associated with poor prognosis and resistance to primary chemotherapeutic treatment in breast, lung, and prostate cancer, as well as glioblastoma and melanoma. Here, AKT1 is linked to glioblastoma.