Their findings demonstrated that binding of FLT3-ITD mutated AML cells to OPN, through integrin αvβ3, could maintain cell survival and induce sorafenib insensitivity by activating the PI3K/Akt/glycogen synthase kinase (GSK) 3β/β-catenin signalling pathway [75]. This evidence concerns the gene AKT1 and acute myeloid leukemia.