For NK cells, this binding does not disrupt oxidative phosphorylation (OXPHOS) or glycolytic pathways— mechanisms that lack support in current NSCLC-focused studies—but instead blocks their maturation process: it reduces the proportion of mature cytotoxic NK cell subsets (e.g. CD27−CD11b+ in murine models, CD56dimCD16+ in humans) and impairs their secretion of interferon-γ (IFN-γ) (a key cytokine that enhances anti-tumour immunity). The gene discussed is IFNG; the disease is neoplasm.