However, a leukemia intrinsic expression of the RET co-receptor is also conceivable as Rudat et al. [47] observed expression of GFRA2 (and the GFRA3 isoform) in human AML cell lines and identified a targetable co-dependency between FLT3-ITD and RET, as the latter suppressed autophagy through mTORC1 activation thereby stabilizing FLT3-ITD. The gene discussed is RET; the disease is acute myeloid leukemia.