Activation of pathways observed in other cancers, such as glioma, glioblastoma, and metastasis in colorectal cancer, was also predicted, and pathways were commonly linked by the inactivation of ATM and CDKN2A and amplification of EGFR. Although epidermal growth factor (EGF) signaling was also predicted to be significantly impacted, it was neither activated nor inhibited due to inactivation of ATM and ITPR1 and amplification of EGFR and JUN. The gene discussed is JUN; the disease is colorectal cancer.