It has also been reported, however, that Mbnl1-knockout mice on a pure 129 sv genetic background (as opposed to Mbnl1∆E3/∆E3 mice, which are on a hybrid background of C57/BL6 and129 strains) exhibit progressive cardiac dysfunction, cardiac hypertrophy, and myocardial cell death and fibrosis despite a similar up-regulation of MBNL2 [82]. Here, MBNL1 is linked to cardiac hypertrophy.