Instead of activating functional effector T cells, UNC93B tended to recruit regulatory T cells, which were responsible for the initiation and development of acute and chronic leukemia (Moon et al., 2011; Bachireddy et al., 2015; Wan et al., 2020), and mediated immune escape of myeloblast in de novo AML (Wan et al., 2020). The gene discussed is UNC93B1; the disease is acute myeloid leukemia.