Beyond impaired differentiation, DLL3 overexpression promotes tumor growth, epithelial-to-mesenchymal transition, and metastasis through the regulation of Snail, Slug, and Twist, and may interact with pathways such as Wnt/β-catenin and PI3K/Akt to enhance tumor survival [31,32,33]. This evidence concerns the gene AKT1 and neoplasm.