One potential scenario that could explain the unique effect of NC525 on AML cells is that LAIR-1 signaling in healthy cells is not apoptotic at homoeostatic levels of mTOR activity, but when aberrant mTOR/AKT/NF-κB activity is driving leukemic self-renewal, the loss of proliferation signal elicited through LAIR-1 cross-linking permits apoptotic self-elimination mechanisms to execute programmed cell death. Here, AKT1 is linked to acute myeloid leukemia.