TARDBP and amyotrophic lateral sclerosis: In general, we can assume that TDP-43 GoF in the cytoplasm is likely implicated in the mechanisms of ALS-associated TDP-43 mutations, but it should be also considered the clear heterogeneity of the phenotype that depend on the expression levels of the mutant protein and/or the genetic background of the animal model (mPrp vs. mTardbp promoter; [109]).