Further investigating the role of PFKL downregulation in the tumor suppressive activity of EGR1 in HCC, we overexpressed PFKL in EGR1-overexpressing PLC/PRF5 cells (Fig. 6A). Through measurements of glucose uptake, extracellular lactate levels, ECAR and ATP levels, our findings indicate that restoration of PFKL expression increased glucose uptake, extracellular lactate levels, glycolysis, glycolytic capacity, and ATP levels in EGR1 overexpressing PLC/PRF5 cells (Fig. 6B-E). The gene discussed is HSPG2; the disease is neoplasm.