While attractive as a mechanism for the suppressed fibronectin secretion in AUY922-treated cells, we detected no consistent change in extracellular vesicle release from multiple PCa cell lines cultured with AUY922, indicating that the defect likely lies either in the integrin-mediated release of MVBs at the plasma membrane or with intracellular trafficking along the microtubule network. The gene discussed is FN1; the disease is posterior cortical atrophy.