ILK is constitutively expressed by AML blast cells and ILK-mediated phosphorylation of Akt and GSK3β downstream of PI3K pathway activation of fms-like tyrosine kinase 3 (FLT-3), a receptor tyrosine kinase (RTK) critical for AML LSC maintenance, controls AML cell survival and proliferation [77]. The gene discussed is ILK; the disease is acute myeloid leukemia.