These effects were recapitulated using an actin-depolymerizing agent, Latrunculin A. Notably, FG-Nup mislocalization in primary neurons from PFN1 transgenic mice, as well as C9orf72-ALS patient fibroblasts, was reversed using an actin polymerization agent, IMM01, suggesting that modulating actin polymerization could modify NCT (Giampetruzzi et al., 2019). Here, C9orf72 is linked to amyotrophic lateral sclerosis.