Although some patients with PD had rapidly decreasing levels of afami-cel persistence, some maintained high levels of persistence, suggesting that tumor-intrinsic factors, possibly immuno-editing mechanisms (for example, loss of MAGE-A4 or HLA expression), or potential immunosuppressive factors (such as arginase-1), might contribute to the development of afami-cel resistance even if afami-cel cytolytic activity can be maintained in vivo. The gene discussed is ARG1; the disease is neoplasm.