SLC2A13 encodes a proton-coupled myo-inositol symporter that mediates cellular uptake of myo-inositol and related stereoisomers. The transporter localizes to multiple cellular compartments including the plasma membrane, synaptic vesicles, and early endosomes, where it supports myo-inositol homeostasis. At the molecular level, SLC2A13 associates with γ-secretase and regulates amyloid-β (Aβ) production in Alzheimer's disease pathogenesis 1. Silencing of SLC2A13 reduces Aβ secretion in a dose-dependent manner, while overexpression increases Aβ40 generation, suggesting a role in substrate selection for γ-secretase-mediated amyloid precursor protein processing 1. Notably, SLC2A13 influences Aβ production without affecting Notch cleavage, offering a potential therapeutic window. In acute myeloid leukemia, high SLC2A13 expression is associated with improved overall survival, with multivariate analysis confirming that elevated expression reduces mortality risk 2. Recent evidence also implicates SLC2A13 in neurodegenerative diseases: rare variants show enrichment in early-onset Parkinson's disease in Chinese populations 3, and genetic polymorphisms in SLC2A13 associate with longer disease duration in progressive supranuclear palsy 4. Additionally, short tandem repeats in SLC2A13 associate with Parkinson's disease risk and modulate penetrance of the LRRK2 G2385R variant 5. A systematic review identified SLC2A13 as one of eight genes showing caffeine-gene interactions in modulating Parkinson's disease risk 6.