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. The gene discussed is LAIR1; the disease is acute myeloid leukemia.