Interestingly, another study by Peng et al. had similar results, showing that monocytes were educated by HCC microenvironment to upregulate their levels of glycolysis, which led to the production of large amounts of CXCL2 and CXCL8 via PFKFB3-NF-κB axis, recruiting peripheral neutrophils, potentially favoring tumor metastasis and facilitating disease progression of human HCC [51]. The gene discussed is NFKB1; the disease is neoplasm.