GBA1 and hyperinsulinemic hypoglycemia, familial, 4: Thus, the excess accumulation of insoluble αSyn in the APOE−/− cerebral organoids may be partially due to the reduction of GBA expression, although further studies are necessary to define the functional link between APOE and GBA. In addition to lipid metabolism, WGCNA also identifies multiple modules affected by apoE deficiency, which include pathways related to plasma membrane metabolism and intracellular organelle transport.