In gliomas, Pan et al. found that circNEIL3 interacts with IGF2BP in the cytoplasm, enhancing the stability of IGF2BP3 protein and inhibiting the E3 ubiquitin ligase HECTD4-mediated degradation of IGF2BP3 at the post-transcriptional level to promote the polarization of macrophage toward an immunosuppressive phenotype enabling gliomas to acquire angiogenic and immunosuppressive properties in turn promoting tumor progression. The gene discussed is IGF2BP3; the disease is neoplasm.