The expression of ALS-PFN1 mutants evokes cytoskeletal and morphological defects in primary neurons, such as abnormally low ratios of F-/G-actin, shorter dendrites and integrity-impaired axons, which undergo Wallerian degeneration over time (Figure 6.2; Wu et al., 2012; Yang et al., 2016; Fil et al., 2017). This evidence concerns the gene PFN1 and amyotrophic lateral sclerosis.