EphA2 is upregulated with grade, promotes ligand-independent, Akt-mediated invasive signaling and supports glioma stem cell self-renewal and tumorigenicity, while EphA3 is enriched in tumor-initiating and mesenchymal compartments and is targetable with CAR T cells and ligand-toxin constructs in preclinical models (Shen et al., 2021; Li et al., 2010; Miao et al., 2015; Suo et al., 2019; Wykosky et al., 2005; Binda et al., 2012; Qazi et al., 2018; Day et al., 2013; Lertsumitkul et al., 2024; Ferluga et al., 2016; Sharma et al., 2020; Wang et al., 2021). Here, AKT1 is linked to neoplasm.