Accordingly, the intriguing link between Ser389 GSK3β deregulation, neuroinflammation, and neurodegeneration unveiled here needs to be further explored to clarify whether altered GSK3β phosphorylation at Ser389 may be a key factor in neuropathologies in which chronic inflammation is distinctive, such as Alzheimer’s disease. The gene discussed is GSK3B; the disease is early-onset autosomal dominant Alzheimer disease.