Oral, selective, allosteric pan-AKT inhibitor that binds the pleckstrin homology (PH) domain of AKT1, AKT2, and AKT3, blocking their membrane recruitment and catalytic activation regardless of AKT mutation status. FDA-approved (November 2023; Truqap) for AKT1/2/3-, PIK3CA-mutated or PTEN-altered HR+/HER2- locally advanced or metastatic breast cancer in combination with fulvestrant (CAPItello-291 Phase 3, NCT04305496). In SDH-deficient tumors, AKT is a primary effector of the pseudohypoxic signaling cascade: SDH loss → succinate accumulation → PHD inhibition → constitutive HIF-1α/2α stabilization → transcriptional upregulation of IGF2 and HGF → IGF1R/MET receptor activation → PI3K/PIP3 generation → AKT recruitment via PH domain → PDK1 + mTORC2-mediated AKT activation → TSC1/2 inhibition → Rheb-GTP → mTORC1 constitutive activation. Jochmanová et al. (JNCI 2013, PMID 23940289) identified this HIF/mTOR/PI3K interconnection as the central tumorigenesis driver in SDH-deficient (pseudohypoxic cluster 1) pheochromocytoma/paraganglioma — the same citation anchoring the everolimus entry. Capivasertib directly addresses the principal pharmacological limitation of everolimus (mTORC1 inhibitor, already in this engine): mTORC1 inhibition removes S6K1→IRS-1 negative feedback, permitting upstream PI3K to drive paradoxical AKT reactivation via mTORC2 and PDK1. Capivasertib prevents this AKT rebound by blocking all three AKT isoforms at the membrane-recruitment step — restoring pathway suppression that single-agent rapalogs cannot sustain. A capivasertib + everolimus combination would simultaneously suppress mTORC1 output and prevent AKT reactivation, a pharmacological rationale directly motivated by the AKT reactivation caveat documented in the everolimus entry. Key limitation: no published experimental data directly test capivasertib in SDH-deficient cell lines or xenografts. The mechanistic rationale rests on the Jochmanová 2013 demonstration of constitutive AKT pathway activation in SDH-deficient PPGL and established rapalog pharmacology, both validated in their respective contexts but not combined in an SDH-specific capivasertib experiment.