Although IFT140 and IFT144 are core IFT-A complex subunits (Mukhopadhyay et al., 2010; Behal et al., 2012) and regulate retrograde trafficking in cilia (Piperno et al., 1998; Iomini et al., 2001; Iomini et al., 2009), the mild polycystic kidney disease phenotype in patients with IFT140 mutations and the lack of cyst suppression in Pkd1; Ift144 double cko with respect to Pkd1 cko could partly arise from pre-ciliary function of the IFT-A core in trafficking TULP3 and its cargoes. The gene discussed is PKD1; the disease is cyst.