Potential upstream regulators could include transcription factors activated by the DNA damage response, such as p53 and NF-κB,49 or post-transcriptional mechanisms such as mRNA stabilization.50,51 Furthermore, the tumor microenvironment, particularly radiation-induced hypoxia or stromal cell interactions, might also contribute to JMJD6 induction, sustaining the resistant phenotype. The gene discussed is NFKB1; the disease is neoplasm.