Mechanistic examination revealed an intricate dynamic protein interaction hub by which LKB1 interacts with IAP in competition with JAK1, which offers a working model that the loss of LKB1 in LKB1-mut cancer cells allows IAP to engage JAK1 to control JAK1-mediated IFNγ response and the effector STING pathway, underpinning the IAP dependency. The gene discussed is STK11; the disease is cancer.