Previous studies inhibiting enhancer of zest homolog 2 (EZH2), which promotes transcriptional silencing downstream, led to elevated expression of DR4 in PCa cell lines, and high levels of NF‐kB in tumor cells have been shown to increase DR4/5 expression.[61, 103, 104] Additionally, Jun N‐terminal kinase activation due to endoplasmic reticulum stress was previously shown to upregulate DR4/5 expression.[27] These findings support the idea that there could be a downstream, yet unidentified mechanism occurring in response to combination treatment that induces an increase in DR5 expression. The gene discussed is NFKB1; the disease is posterior cortical atrophy.