The signature of these neutrophils was positively correlated with the global profile of PMN-MDSCs and TANs [138]; however, in another study, it was demonstrated that a strong affinity of M-MDSCs towards tumor cells resulted in the induction of the EMT/CSC phenotype through activation of both STAT1 and STAT3 signaling pathways in tumor cells, accounting for the upregulation of EMT-related genes such as vimentin, CK14, and Twist. The gene discussed is STAT3; the disease is neoplasm.