This disconnect may indicate that CAMK1/CREB is dispensable for AML cell survival in the context of collagen matrices, where the LAIR-1 signaling network suppresses alternative downstream mediators, such as NF-κB, MAPK, and Src family kinases, to the point that the signaling threshold overcomes prosurvival mechanisms to instead result in programmed cell death. This evidence concerns the gene NFKB1 and acute myeloid leukemia.