Specifically, expression of expanded CUG repeat sequences results in elevated steady-state CUG-BP1 protein levels, which plays a causative role in dysregulating splice site choice in a set of physiologically important RNAs implicated in DM1 both in cell culture and transgenic mouse experiments [25], [33], [39], [45]–[49]. The gene discussed is CELF1; the disease is myotonic dystrophy type 1.