Researchers from The Hebrew University of Jerusalem reported that blocking neuronal nitric oxide synthase (nNOS) suppresses neuroblastoma growth by disrupting an AKT–TSC–mTOR signaling cascade. The group combined findings from human neuroblastoma cells with a mouse xenograft model and reported tumor growth suppression after nNOS inhibition. The work, published in Brain Medicine, frames the nNOS–mTOR axis as a therapeutic target, with nitric oxide positioned as a regulatory driver of carcinogenesis in neuroblastoma biology. Senior author Haitham Amal said the results identify a pathway that could be therapeutically exploited for high-risk disease. Given neuroblastoma’s pediatric burden and relapse risk, the pathway-level mechanism may guide future target validation and combination strategies aimed at widening treatment windows.