IFNG and neoplasm: Accumulated adenosine activates the A2A receptor (A2AR) on T cells, suppressing TCR signaling, reducing IFN‐γ production, and promoting T cell exhaustion and Treg induction—constituting a major axis of immunosuppression.[155, 156] Additionally, nucleotide pool imbalances in immune cells under nutrient stress or tumor‐induced metabolic competition can lead to DNA replication stress and ATR/Chk1 pathway activation, culminating in cell cycle arrest or apoptosis.[157] These processes compromise effector T cell function and facilitate immune escape.[158]