The TME can also evoke the overexpression of Nrf, a redox-sensitive transcription factor, inhibiting DC functional maturation.86 Tumor-derived VEGF can inhibit the activity of FMS-related tyrosine kinase 3 ligand (FLT3L), crucial for in-situ DC development and survival.87 Low extracellular nutrients and a high AMP/ATP ratio in the TME can activate AMP-activated protein kinase (AMPK) in DCs, leading to the expression of tumor-promoting factors such as VEGF, TGF-β, and IL-10.88 Other cell types also modulate the DCs. Here, FLT3LG is linked to neoplasm.