Although the exact mechanism for this phenomenon is not known, we speculate that it may be mediated by the transcription factor HIF1α, since there is recent evidence from a neuroblastoma cell line that the HIF1α transcript is up‐regulated or down‐regulated following calreticulin up‐regulation or down‐regulation.37 We have confirmed this finding in our renal tubular epithelial cell line, where we have observed a 10‐fold increase in the HIF1α transcript when calreticulin is overexpressed (data not shown). The gene discussed is CALR; the disease is neuroblastoma.