Conditional knockout of Glut1 in neutrophils increases TAN turnover and reduces accumulation of SiglecF+ TANs in the TME delaying tumor growth and sensitizing them to radiotherapy.62 These observations emanating mostly from mouse models suggest that tumor-promoting neutrophils, as exemplified by SiglecF+ TAN and immunosuppressive neutrophils are referring to different types of cells, each of them contributing to disease progression and refractoriness to treatment. The gene discussed is SLC2A1; the disease is neoplasm.