The complete loss of Flii has been shown to be embryonically lethal in mice, with failure of egg cylinder formation prior to gastrulation (Campbell et al., 2002) and human Flii maps within the critical region of chromosome 17 where contiguous-gene-deletion gives rise to the Smith-Magenis syndrome, the clinical features of which include short stature, brachydactyly, developmental delay, dysmorphic features, sleep disturbances, and behavioral problems (Chen et al., 1995). The gene discussed is FLII; the disease is Global developmental delay.