Neurolysin (NLN) is a mitochondrial metalloendopeptidase that primarily functions as a peptide hydrolase with emerging oncogenic roles. While traditionally characterized as degrading neuropeptides through metalloendopeptidase activity, recent evidence reveals NLN's critical involvement in ferroptosis regulation and cancer progression. In non-small cell lung cancer (NSCLC), NLN expression is significantly elevated compared to normal lung tissue, and NLN inhibition induces ferroptosis through suppression of m6A methylation-mediated GPX4 mRNA degradation, effectively suppressing tumor growth in vivo 1. This ferroptosis-regulatory mechanism represents a previously unrecognized function distinct from NLN's classical role as a neuropeptide-degrading enzyme. The discovery of specific NLN inhibitors (such as NR2) that induce tumor cell death positions NLN as a promising therapeutic target for NSCLC and potentially other malignancies 1. These findings establish NLN as a crucial regulator of cell death pathways beyond its characterized peptide hydrolysis activity, providing a novel mechanistic basis for cancer therapeutics development and addressing challenges of drug resistance and tumor progression.