Having shown that SGs are not present in DM1 HLECs under normal growth conditions – suggesting that any increase in basal stress levels is insufficient to drive SG formation – and that SGs containing MBNL1 and CUGBP1 are readily formed in response to NaAsO2, we next sought to investigate the kinetics of SG formation and SG loss in DM1 HLECs compared to control cells. The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.