Although phenotypes similar to neutrophils manifest CD11b+/Ly6G+/Ly6Clow in mice and CD14−/CD11b+/CD15+ (CD66b+) in humans [119], functional annotations and transcriptomic analysis have defined their distinctions: TANs exhibit tumor-promoting roles by exerting innate immune inflammation; CCL2 and CCL17 secreted by TANs recruit peripheral monocytes to further differentiate into TAMs and Tregs to suppress effective antitumor immunity, as described above [120,121], and PMN-MDSCs promote tumor progression by suppressing adaptive immune response via inhibiting T-cell function [122]. The gene discussed is FUT4; the disease is neoplasm.