Since NIN is involved in regulating cellular architecture and mitotic processes, it may be particularly susceptible to stress conditions, especially if HSPs that interact with centrosomal proteins are affected.9 While no significant RMSD changes were observed in the structural analysis, the localized hydrophobicity changes and the involvement of stress-response pathways suggest that the NIN-CEP170 complex may be less able to cope with cellular stress, potentially contributing to developmental defects such as microcephaly and growth retardation. This evidence concerns the gene CEP170 and microcephaly.