The molecular mechanisms include the release of damage-associated molecular patterns (DAMPs), the activation of NFkB signaling, a higher PD-L1 expression on tumor cells, an increase in CD8+ T-cells, the maturation of antigen-presenting cells (APC), augmented antigen presentation through MHC-I and the downregulation of immunosuppressive cells at the tumor site (Treg and myeloid-derived suppressor cells). Here, NFKB1 is linked to neoplasm.