Furthermore, a defect in SG formation in response to treatment with sodium arsenite (NaAsO2) has been reported in DM1 patient-derived fibroblasts expressing exogenous MyoD to mimic a myoblast phenotype, suggesting impaired ability of DM1 cells to respond to stress (Ravel-Chapuis et al., 2016).Here, we identified both MBNL1 and CUGBP1 as components of P-bodies as well as SGs in human lens epithelial cells (HLECs) and in a novel inducible cell model of DM1. This evidence concerns the gene CELF1 and myotonic dystrophy type 1.