However, the mutation in CHMP2B intron5 was recently implicated in the hyperphosphorylation of TDP-43 via the ubiquitin-proteasome system (UPS), decreasing ubiquitination and turnover of casein kinase 1 (CK1), highlighting a genetic link between TARDBP and CHMP2B and the associated ALS pathology [77]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.