Schematic representation of the pathogenic mechanisms of CDAs at the subcellular level. (A) Pathogenic mechanisms of CDAs I and II, and of the transcription-factor-related CDAs at the erythroblast level, with schematic representation of erythroblasts and the roles of the causative proteins in the different subcellular compartments. SEC23B is a COPII component that is involved in anterograde transport from the endoplasmic reticulum toward the Golgi compartment. Moreover, SEC23B is involved in autophagy. The pathogenic mechanisms of transcription factor-related CDAs and CDAIa and Ib arise from impairment of mechanisms involved in DNA synthesis and chromatin assembly. During cell division, GATA1 and KLF1 might be retained focally within mitotic chromatin to facilitate the rapid reactivation of the transcription of tissue-specific genes upon entry into G1; codanin-1 and C15orf41 interact with the cytosolic Asf1–H3–H4–importin-4 complex that is involved in nucleosome assembly and disassembly. (B) The pathogenic mechanisms of CDAs I, II, and III at the erythroblast level, with schematic representation of cell division and the roles of the causative proteins in the different mitotic stages. C15orf41 encodes a protein with homology to the Holliday junction resolvases, which are involved in chromosome segregation. The KIF23 mutant results in furrow regression, and thus inhibits cytokinesis. SEC23B has a crucial role in the assembly or deconstruction of the midbody during cytokinesis.