Cryptic exons that emerge in human models of TDP-43 loss of function are not recapitulated in mouse models (Ling et al., 2015; Humphrey et al., 2017), including a cryptic exon identified in STMN2 that has attracted significant attention in ALS/FTD research (Klim et al., 2019). This evidence concerns the gene STMN2 and amyotrophic lateral sclerosis.