KDM2B has been previously shown to be nuclear factor (NF)-κB dependent, and be negatively regulated by TRAIL treatment in several cancer cell lines . While we have previously shown that hypoxia activated NF-κB to modulate its targets , we have not investigated if hypoxia-induced KDM2B mRNA is NF-κB dependent. We did find that depletion of HIF-1 significantly decreased KDM2B mRNA in hypoxia. Moreover, recently, we demonstrated that HIF-1α acts as a repressor of NF-κB in cells, controlling its activity both in normoxia and hypoxia , thus suggesting that under these conditions, NF-κB does not control KDM2B expression. Intriguingly, hypoxia exposure results in reduced protein levels of KDM2B in U2OS, in a HIF-1-dependent manner, suggesting that HIF-1-mediated effects on KDM2B protein are not direct and are post-transcriptional. How KDM2B protein is regulated in U2OS cells is currently unknown and would thus require additional work.