In fibroblasts of a ciliopathy patient with short rib polydactyly, mutation of IFT52 greatly reduced IFT52 protein levels, leading to a destabilized anterograde IFT complex, demonstrated by reduced cellular levels of IFT88, IFT74, IFT81, and ADP ribosylation factor like GTPase 13B (ARL13B), a ciliary membrane protein, as well as reduced IFT88 in cilia (Zhang et al., 2016). The gene discussed is IFT88; the disease is ciliopathy.