The discovery that the translocation of the ER chaperone—calreticulin (CRT) to the cell surface of some tumour cells, where it acts as a ‘eat-me’ molecule [4], may enhance the immunogenicity of early apoptotic cancer cells by triggering both innate immunity (phagocytosis and a specific adaptive immune response termed immunogenic cell death (ICD) [5], has drawn attention to CRT for aiding cancer cell recognition by the immune system in recent years [6–9]. The gene discussed is CALR; the disease is neoplasm.