Subsequently, using a SCC-25 oral cancer–derived CSC model, we showed that hypoxia/reoxygenation or chemotherapy-induced TS enables ABCG2-positive sub-fraction of EpCAM+/ALDH1+/CD44v3+ CSCs to modulate TME for rapid tumor progression and immune suppression (11, 12). Here, EPCAM is linked to neoplasm.