Absence of ciliary movement or altered ciliary beating, respectively, and reduced particle transport as surrogate for MCC, as well as altered cilia ultrastructure compared to hiPSC-derived WT airway cells could be confirmed in PCD patient hiPSC-derivatives carrying mutations in DNAH5 [9], encoding for a protein of the outer dynein arm, and NME5 [7], encoding for a protein of the radial spoke. The gene discussed is DNAH5; the disease is primary ciliary dyskinesia.