Thus, the sequestration of MBNL1 by mutated RNAs and the steady-state level of CELF1 in DM1 tissues reproduces the fetal level of these factors, leading to a fetal-type pattern of splicing [recently reviewed in Lee and Cooper (2009), Mastroyiannopoulos et al. (2010), Klein et al. (2011)]. This evidence concerns the gene MBNL1 and myotonic dystrophy type 1.