These mechanisms include the generation of tumour-associated antigenic peptides through cell death and the release of “danger signals”, including major histocompatibility class I surface expression, which is up-regulated in a dose dependent fashion, via mTOR activation to subsequently present tumour antigens to the cell surface for recognition by CD8-positive T cells [27]; calreticulin expression, which promotes phagocytosis [28]; and the release of high-motility group box 1 (which stimulates the immune response via toll-like receptor 4 [29]). Here, CALR is linked to neoplasm.