Failure of chromosomes to integrate into newly forming daughter nuclei after cell division leads to the formation of micronuclei. These micronuclei have reduced levels of DNA damage repair and therefore accumulate DNA lesions. Upon reintegration of the micronuclei during subsequent cell divisions, DNA damage can lead to large structural rearrangements of chromosomes, or chromothripsis, a hallmark of cancer cells. Here, Jonne Raaijmakers and co-workers (Soto et al., 2018) investigate the fate of cells with micronuclei. They show that chromatids from micronuclei are misaligned in metaphase and have high mis-segregation rates upon anaphase onset. In addition, these chromatids do not have an active spindle assembly checkpoint and show low levels of kinetochore assembly proteins. Strikingly, when followed through long-term live-cell imaging, micronuclei exclusion appears to be favoured over reintegration into the daughter nuclei. Thus, the defects in kinetochore protein levels contribute to a delay in the propagation of defective or excess chromosomes, as reincorporated micronuclei overcome their defects and propagate normally. These findings provide evidence for the long-term fate of micronuclei during cell division and suggest a control mechanism to exclude faulty chromatids and prevent subsequent chromothripsis.