Slc2a13, also known as the proton myo-inositol cotransporter, is a member of the solute carrier family 2. It plays a role in the transportation of myo-inositol along with protons across cell membranes. It is associated with the γ-secretase complex, and thus is involved in the processing of amyloid precursor protein, which is related to the pathogenesis of Alzheimer's disease. Additionally, as a solute carrier, it may be related to nutrient transport and metabolism-related pathways in cells [1].

In Alzheimer's disease research, silencing of Slc2a13 led to a clear reduction of amyloid β-peptide (Aβ) secretion in a small interfering RNA dose-dependent manner. Overexpression of Slc2a13 increased Aβ40 generation. Also, the interaction between γ-secretase and Slc2a13 was confirmed, suggesting it could be a target for Aβ-lowering therapy [1].

In acute myeloid leukemia (AML), patients with high Slc2a13 expression exhibited a better prognosis, indicating its potential as a prognostic biomarker [2].

In oral squamous cell carcinoma, Slc2a13 was identified as a potential marker for cancer stem cells as it was over-expressed in sphere-forming cells which are enriched with potential CSCs [3].

In Parkinson's disease, genetic association studies showed that there is a caffeine-gene interaction involving Slc2a13 which may influence the risk of PD, and a 5-copy GGGAAA repeat in Slc2a13 was significantly associated with PD [4,5].

In conclusion, Slc2a13 has diverse functions in different biological processes and disease conditions. Its role in regulating Aβ production in Alzheimer's disease, as a prognostic biomarker in AML, as a potential cancer stem cell marker, and in the gene-caffeine interaction in Parkinson's disease, is of great significance. Functional studies, especially those using gene knockout or conditional knockout mouse models in the future, may further clarify its molecular mechanisms in these diseases.