The ATF/CREB family of proteins interacts with multiple domains of CREB‐binding protein (CBP), which are functionally essential for other transcription factors, such as NF‐κB, TP53, and STATs.[27, 28] Knockout of ATF4 significantly decreased the expression of the noncanonical NF‐κB pathway components in cancer cells (Figure 6H, upper panel of Figure 6J), whereas overexpression of ATF4 increased the corresponding expression of these noncanonical NF‐κB pathway components (Figure 6I, lower panel of Figure 6J), with nuclear translocation of RelB and p52 (Figure 6K). The gene discussed is NFKB1; the disease is cancer.