The same research group provided solid fly-based evidence for the still controversial contribution of CELF1 to DM1, focusing on the muscle-specific overexpression of Bru-3, the Drosophila CELF1 family member, which contributes to pathogenic muscle defects similar to those seen in humans, including affected motility, fiber splitting, reduced myofiber length, and altered myoblast fusion [73]. This evidence concerns the gene CELF1 and myotonic dystrophy type 1.