LILRB1 and acute myeloid leukemia: In a study performing transcriptional profiling of different molecular subtypes of AML‐CTLs, upregulation of inhibitory molecules (CD244, CD160, LILRB1, CD300A, LAG3, TIGIT, PVRIG) and downregulation of stimulatory molecules (CD40LG, CD28, ICOS, TNFSF8, TMIGD2, TNFRSF25) were identified as compared to CTLs from healthy controls.4