Viral infection of tumor cells triggers the release of damage-associated molecular patterns (DAMPs)—including Adenosine Triphosphate (ATP), high mobility group box 1 (HMGB1), and calreticulin—which activate dendritic cells and enhance tumor antigen presentation, eliciting specific CD8+ T-cell responses and transforming immunologically “cold” tumors into “hot” tumors [19,20]. This evidence concerns the gene CALR and neoplasm.