The temporary activation of cofilin through dephosphorylation facilitates the insertion of AMPAR at the synapse terminal, and the inactivation of cofilin via LIMK-mediated cofilin phosphorylation allows the enlargement of dendritic spines, enabling the dynamic regulation of synaptic plasticity and spine morphology in HD, AD, and stroke [51]. This evidence concerns the gene CFL1 and Huntington disease.