Building on the known activity of ACTN4 as a transcriptional coactivator of the RelA/p65 subunit of Nuclear factor-κB [53], Ji et al. could demonstrate that the SChLAP1–HNRNPL complex indeed promoted transcriptional activity and nuclear translocation of Nuclear factor-κB via enhancing ACTN4 stability in glioblastoma cells. The gene discussed is ACTN4; the disease is glioblastoma.