The epigenetic modification function of unphosphorylated STAT3 was also identified by Timofeeva1 who suggested that cancer cells such as DU145 and MCF-7 cells have a more open or, at least, more accessible chromatin conformation than the non-transformed MCF-10A cells, thereby allowing for unphosphorylated STAT3 binding, suppression of CHOP expression, and subsequent inhibition of the apoptosis of cancer cells with the involvement of the N-terminal domain of STAT3. The gene discussed is DDIT3; the disease is cancer.