PP2A exhibits a context-dependent duality in cancer biology, functioning as both a tumor suppressor through its phosphatase-mediated inactivation of growth-promoting kinases (e.g., PI3K/AKT and MAPK/ERK) and MYC-driven transcription and as a potential tumor promoter when its regulatory subunits are hijacked to stabilize survival pathways or when specific holoenzyme complexes paradoxically enhance oncogenic signaling networks (Fig. 4) [104, 178, 179]. Here, MYC is linked to neoplasm.