INSR and myotonic dystrophy type 1: This result suggested the use of a cryptic 3′ splicing site in the human INSR intronic sequence, perhaps because of the different accessibility to a human sequence of the alternative splicing machinery present in Drosophila. At the same time, no differences were detected in the splicing outcome (exon 11 skipping) between human and flies after the sequence analysis of isoform A (predominant in the DM1 state when muscleblind proteins are sequestered by CUG repeats).