Although accumulating inhibitors targeting the NF‐κB pathway have been approved for inflammatory diseases, and explored for cancer therapy in clinical trials,[33] the cell toxicity and immune‐related side effects limit their usage in combating cancer.[34, 35] One possible reason for this limitation is the elevation of CTR1 and copper uptake, leading to activation of MAPK and AKT pathways, resulting in resistance to NF‐κB inhibitors such as QNZ. The gene discussed is AKT1; the disease is cancer.