Indeed, intraventricular administration of AAVs carrying dominant-negative Sarm1 constructs driven by the human Synapsin promoter (AAV8-Syn-SARM1-CDN-eGFP) at the time of tumour induction resulted in axonal protection and reversed effects of transection injury at the intermediate disease stage, relative to AAV8-Syn-EGFP-injected controls (Extended Data Fig. 6a–f). This evidence concerns the gene NT5C and neoplasm.