The suitability of our Drosophila DM2 system as a disease model was further demonstrated by the observation that different spliceosensor luciferase reporters, which express specific mammalian reporter mini-genes for identified mis-splicing events in DM1 and DM2 (human INSR exon 11 and mouse Tnnt3 fetal exon) (Savkur et al., 2004; Vihola et al., 2010; García-Alcover et al., 2014), were also responsive to the presence of expanded CCUG repeats (Fig. 2F,H). The gene discussed is INSR; the disease is myotonic dystrophy type 1.