Hence, we suggest that HuR overexpression stimulates the proinflammatory cellular composition of the glioma microenvironment, which provides positive feedback for HuR overexpression and nuclear/cytoplasmic shuttling in glioma cells and is associated with cell fusion and tunneling nanotube formations, which favor the development of glioma heterogeneity and treatment resistance. The gene discussed is ELAVL1; the disease is glioma.