AKT1 and neoplasm: Additionally, mTORC1 signaling, glycolysis, TGF‐β signaling, PI3K/AKT/mTORC signaling, hypoxia, TNF-α signaling via NF-κB, and angiogenesis were enriched in tumor ECs, suggesting the involvement of EndMT ECs in angiogenesis induction in HPSCC (Fig. 4g) [41–43].