TARDBP and amyotrophic lateral sclerosis: Alternative splicing defects, particularly impaired repression of cryptic exons, due to TDP-43 dysregulation are strongly implicated in FTLD and ALS pathogenesis (Melamed et al., 2019; Ma et al., 2022; Ling et al., 2015; Arnold et al., 2013; Prudencio et al., 2020; Humphrey et al., 2017).