Other familial ALS mutation phenotypes, such as valosin-containing protein (VCP) (Hall et al., 2017), TAR DNA-binding protein 43 (TDP-43) (Serio et al., 2013; Barmada et al., 2014), and superoxide dismutase (SOD1) (Bhinge et al., 2017), have been recapitulated in iPSCs showing characteristic proteinopathies, and endoplasmic reticulum (ER) and oxidative stress. This evidence concerns the gene TARDBP and proteostasis deficiencies.