Compared with direct NO gas delivery or synthetic NO donors (e.g., nitrates, S‐nitrosothiols), L‐Arg produces NO through endogenous enzymatic pathways, enabling slower and more controllable release while avoiding excessive NO‐induced cytotoxicity and oxidative stress.[12] In the tumor microenvironment (TME), L‐Arg can be catalyzed by inducible NOS (iNOS) and activated under tumor‐specific conditions (e.g., high H2O2 levels) to achieve localized NO release, thereby promoting vasodilation, alleviating tumor hypoxia, improving ROS generation efficiency in PDT, and enhancing tumoricidal effects. This evidence concerns the gene NOS2 and neoplasm.