Additionally, neutrophils can suppress cytotoxic T-cell responses through various mechanisms, such as the secretion of arginase-1 and reactive oxygen species, thereby reducing the immune system’s capacity to effectively target and eliminate tumor cells.[18,19] This inflammatory environment likely contributes to the limited efficacy of ICI therapy observed in patients with higher dNLR levels, as ICIs rely on robust T-cell activity to mediate their antitumor effects. The gene discussed is ARG1; the disease is neoplasm.