During later stages, glial cells' impaired phagocytic function certainly plays a role in the worsening of disease outcomes, although the underlying mechanisms are yet to be understood.[23] Hence, to stop plaque formation and activation of proinflammatory cytokines and related consequences, it is crucial to comprehend AD‐related molecular processes that underlie glial phagocytosis, Aβ degradation, and microtubule stabilization with probable roles of HDAC6 for the advancement of AD therapeutics. The gene discussed is HDAC6; the disease is Alzheimer disease.