As the largest structural component of the IFT-B protein complex, IFT172 is involved in anterograde transportation and thus frequently engaged in diseases including related ciliopathies, growth hormone deficiency, non-syndromic retinitis pigmentosa, MKS, and Mainzer-Saldino syndrome (MZSDS) (Bujakowska et al., 2015; Schaefer et al., 2016; Wang et al., 2018; Pruski et al., 2019). This evidence concerns the gene IFT172 and short-rib thoracic dysplasia 9 with or without polydactyly.