This mechanism explained the effects of azacytidine and anti‐CD47 in cases of myelodysplastic syndromes and acute myeloid leukaemia since the hypomethylating agent was shown to upregulate calreticulin levels on cancer cells, thus predominantly boosting prophagocytic signals when DEMs is abated by anti‐CD47.28, 29. The gene discussed is CALR; the disease is myelodysplastic syndrome.