Similarly, TNS4 (CTEN) functions as an oncogene in colorectal cancer and lung adenocarcinoma, where its overexpression promotes epithelial–mesenchymal transition, migration, invasion, aerobic glycolysis, and tumor growth through upregulation of glycolytic genes (HK2, LDHB, PKM, SLC2A1) and activation of β-catenin/c-Myc and EGFR signaling pathways, contributing to poor prognosis and drug resistance [113], [114]. Here, MYC is linked to neoplasm.