Under stress, cells release endogenous huntingtin from the ER into the nucleus and localize to nuclear actin-cofilin rods, facilitating actin dynamics; however, mutant huntingtin localization to these rods does not allow for restoration of actin and instead produces a persistent phenotype in rods that resemble cytoplasmic rods in AD pathology (Munsie et al., 2011). This evidence concerns the gene CFL1 and Alzheimer disease.