Besides RANKL, increased UPR signaling stimulated the expression of VEGF and TNF, consistent with previous studies in neuroblastoma cells and macrophages.59, 60 Furthermore, inhibitors of either Perk or Ire1a activity blunted the Tm‐induced increase in RANKL mRNA in cultured cells, thus linking the UPR with RANKL transcription. The gene discussed is ERN1; the disease is neuroblastoma.