The hypothesis of premature differentiation postulated during ZIKV infection, associated with an imbalance in centrosomal proteins, has also been supported by Gabriel et al. [89], who, after infecting NPC cells, found alterations in the recruitment of the centrosomal proteins CEP-152, pericentrin (PCNT), and centrosomal P4.1-associated protein (CPAP), as well as a reduction in the levels of CEP-164. Here, CEP152 is linked to Zika virus infectious disease.