The in vivo role of the antagonistic p53/NF-κB crosstalk for cancer development was shown in a mouse model of KrasG12D-driven lung adenocarcinoma, where loss of p53 triggers NF-κB activation essential for tumor development, whereas restoration of p53 in established p53-null lung tumors leads to NF-κB inhibition and tumor suppression [94]. The gene discussed is NFKB1; the disease is cancer.