Studies suggest that the majority of symptoms in DM1 are a result of a toxic RNA gain-of-function caused by the accumulation of mutant DMPK RNA in ribonuclear foci in the nucleus, resulting in the sequestration of MBNL1 (Miller et al., 2000; Mahadevan et al., 2021), which is brought on by the expanded CUG repeat (Lee and Cooper, 2009; Chau and Kalsotra, 2015). Here, MBNL1 is linked to myotonic dystrophy type 1.