AKT1 and neoplasm: For example, TECs can be transdifferentiated and formed by inducing tumor cells, CSCs, or vascular progenitor cells (VPCs) through mechanisms such as autophagy, and ROS activation of Akt/inhibitor of kappa B kinase (IKK) signaling pathways, such as CSCs of glioblastoma, breast, and ovaries all can differentiate into ECs in morphology and function [242, 243, 251, 252].