Overexpression of C/EBPβ exacerbates the pathological features of AD, primarily by promoting neuroinflammation and mediating the transcriptional regulation of key molecular pathways, including δ‐secretase, apolipoprotein E4 (APOE4), acidic leucine‐rich nuclear phosphoprotein‐32A (ANP32A), transient receptor potential channel 1 (TRPC1), and Forkhead BoxO (FOXO). The gene discussed is CEBPB; the disease is Alzheimer disease.