Moreover, TDP-43 regulates the splicing of non-conserved cryptic exons which are spliced into messenger RNAs in the absence of TDP-43, and the repression of cryptic exons is impaired in ALS-FTLD cases, suggesting that the splicing defect potentially underlies TDP-43 proteinopathy [36]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.