The rationale for applying ATAC‐seq profiling to primary human AML samples was the aim to detect subtle changes in lowly abundant TF activities that might not be detectable by RNA‐seq to identify the network underlying the very poor outcome of AML with high GPR56 expression (Pabst et al, 2016; Garg et al, 2019) including TFs upstream of GPR56. Here, ADGRG1 is linked to acute myeloid leukemia.