IFNA1 and neoplasm: The mechanisms by which these epi-therapies exert their activity are not fully elucidated, but it has been suggested that they may involve reactivation of ERVs, upregulation of tumor-surface antigens, stimulation of antigen-presenting mechanisms, activation of IFN response pathways, transcriptomic reprogramming of TME cells, or induction of immune checkpoint blockade targets such as PD-1/PD-L1 on both tumor cells and lymphocytes alongside reversal of T cell exhaustion [79].