CALR and neoplasm: This process is characterized by cell–surface translocation of CRT as mentioned above, extracellular release of adenosine-5′-triphosphate (ATP) and high mobility group box 1 protein (HMGB1)/receptor of advanced glycation end-products (RAGE), chemokine release and stimulation of type I interferon (IFN) responses [42,43,44], the latter mediated in part via the interaction of damaged nucleic acid originating from dead and dying tumor cells with nucleic acid-sensing TLRs expressed on neighboring, viable tumor cells [42,43,44,45,46].