CALR is expressed at abnormally high levels on the cell-surface of a wide variety of cancer cells, including some hematological malignancies (Wemeau et al., 2010; Zamanian et al., 2013, 2016), suggesting that, by antagonizing the “eat-me” signal provided by CD47, CALR may promote disease progression via inhibition of the surveillance by the immune system (Obeid et al., 2007; Chao et al., 2010). This evidence concerns the gene CALR and hematologic disorder.