In BRAF inhibitor-resistant melanoma cells, upregulation of AEBP1 mediated by hyperactivation of the PI3K/Akt-CREB (cAMP response element-binding protein) pathway activated NF-κB activity by accelerating IκBα degradation, thereby conferring acquired resistance to BRAF (V600E) inhibition16. The gene discussed is BRAF; the disease is melanoma.