CALR and neoplasm: First, reticulum stress leads to cell surface exposure of calreticulin (CRT).[4] This “eat me” signal promotes tumor cell phagocytosis by dendritic cells, which are then activated by ATP and high mobility group box 1 release.[5,6] Then, type I Interferon (IFN) release could induce CXCL10 secretion and CD8+ T cell homing in the tumor microenvironment.