A recent study [16], investigated the effects of overexpressing LIMK1 in the hippocampal excitatory neurons of APP/PS1 mice, a commonly used model for AD, which exhibits significant reduced levels of phosphorylated cofilin [16], potentially leading to destabilization of the actin cytoskeleton and contributing to synaptic degradation. The gene discussed is LIMK1; the disease is Alzheimer disease.