CELF1 and myotonic dystrophy type 1: Concurrently, pathological overexpression of multiple RBPs, such as CUG-BP and ETR-3-like factors (e.g. CELF1) and HNRNPA1, drives the reversion to foetal splicing patterns observed in adult myotonic dystrophy type 1 tissues.9-12 The dysregulation of these RBPs leads to abnormalities in alternative splicing (AS) of many pre-mRNA products and a shift towards foetal splicing patterns in the adult state.13,14