In a previous study, we identified using affinity purification mass spectrometry (AP-MS) and proximity biotinylation (BioID) assays that TBC1D9 interacts with ARL8A and PLK1, and we hypothesized that, by restraining the expression of these genes, TBC1D9 might mediate its effect as a tumor suppressor by inhibiting cell division, migration, and extracellular matrix remodeling [7]. The gene discussed is ARL8A; the disease is neoplasm.