The increased cellular migration and anchorage-independent growth we observed upon silencing of ATP6AP1 or ATP6AP2 indicates that loss of function of either gene results in the acquisition of oncogenic properties in vitro, supporting a novel tumor suppressor role for ATP6AP1 and ATP6AP2 and the notion that inactivating mutations targeting these genes are potential drivers of GCTs. This evidence concerns the gene ATP6AP1 and neoplasm.