More recently, it was shown that truncated MBNL1 overexpressed from the AAV vector, which preserved both ZFs tandems but is deprived of the C-terminal domain, binds to the CUGexp with high affinity, leading to the release endogenous MBNL proteins from sequestration and then rescue of disease phenotypes in the DM1 mouse model.31 Here, MBNL1 is linked to myotonic dystrophy type 1.