FUS and amyotrophic lateral sclerosis: For example, FUSΔNLS mice express a truncated FUS protein lacking the nuclear localisation signal (NLS), with floxed exons 13 and 14 followed by stop codons and a polyadenylation signal, allowing Cre-mediated reversal of the MN loss phenotype, giving new insight into the potential effects of ALS therapies at different disease stages (Scekic-Zahirovic et al., 2016) (Table 1C).