A new mechanistic study identifies a neuroblastoma survival pathway that may be druggable by disrupting neuronal nitric oxide synthase (nNOS) signaling. Researchers from The Hebrew University of Jerusalem reported in Brain Medicine that blocking nNOS suppresses AKT–TSC–mTOR signaling and slows neuroblastoma growth. The team combined work in human neuroblastoma cells with experiments in a mouse xenograft model to connect nitric oxide production to mTOR-driven tumor biology. With high-risk neuroblastoma still associated with poor prognosis and frequent relapse, the nNOS–mTOR axis adds a specific targetable node aimed at reducing therapy resistance biology rather than only shrinking tumors.