Cholesterol metabolism plays a pivotal role in tumor progression and the regulation of the immune microenvironment.[46] Multiple studies have reported that cholesterol and its metabolites can establish an immunosuppressive microenvironment and attenuate the antitumor effects of CD8+ T cells, macrophages, neutrophils, and so on.[47, 48] In this study, we found that the addition of exogenous cholesterol or overexpression of SREBF2 reversed the polarization of neutrophils toward the antitumor phenotype induced by CXCL2 overexpression. The gene discussed is CXCL2; the disease is neoplasm.