Kinome profiling of NF2-null meningioma models revealed activation of Eph receptors (EPHA2, EPHB1), c-KIT and Src family kinases that are inhibited by dasatinib, but mTORC1/2 signaling remained active and limited monotherapy efficacy; parallel studies showed NF2 loss drives autocrine NRG1-ERBB3 signaling that crosstalk with EphA2 and mTORC1/2, and that mTORC1/2 inhibition triggers compensatory pAkt T308 activation via IGF1R/insulin receptor which is only abrogated by combined mTORC1/2 and IGF1R/insulin blockade (Angus et al., 2018; Beauchamp et al., 2021). The gene discussed is INS; the disease is meningioma.