Two mechanisms involving AML immune evasion have been identified, one of which is mainly mediated by CD14+ monocyte-like AML through the LILRB4/SHP-2/NF-κB/uPAR/ARG1 signaling pathway (Deng et al., 2018; van Galen et al., 2019), which is inconsistent with the low expression of CNST in monocytes. The gene discussed is CNST; the disease is acute myeloid leukemia.