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Cancer cells promote LD formation through lipid metabolic reprogramming driven by oncogenic signaling and microenvironmental stress through multiple mechanisms: (i) Oncogenic PI3K/AKT/mTOR signaling activates SREBP, which in turn upregulates de novo lipogenesis through expression and functional activation of downstream target genes ( ATP-citrate lyase/ACC/FASN ), and cholesteryl esterification, expanding the neutral lipid pool that feeds LD biogenesis, particularly in Akt-driven tumor contexts such as glioblastoma 23,24,25