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The proposed mechanisms could lie in the ability of melatonin to regulate, through its receptor MT1, the transcription of the tumor suppressor gene p53, increasing the cell cycle inhibitor p27 (kip1) and the consequent activation of protein kinases (PK) A (PKA), and C (PKC) [28,39]

This signal 4 also presents a new opportunity for therapeutic intervention, and treatments that metabolically rewire T cells, tumor cells, or other cells in the TME have the potential to improve anti-tumor immunity