A number of Seckel syndrome disease genes including ATR, ATRIP, DONSON and TRAIP have well-established roles in the response to RF-stalling (73–77), and their dysfunction provides an explanation for intrauterine and postnatal growth defects based on incomplete chromosome replication, cell-cycle arrest, and a general defect in cell proliferation during development (78). The gene discussed is TRAIP; the disease is Seckel syndrome.