Models for anaphase error correction mediated by an Aurora B activity gradient at the spindle midzone. Model 1: Upon leaving the centromeres, Aurora B establishes an activity gradient at the midzone and phosphorylates specific kinetochore substrates, like pKnl1 (Ser24), leading to the destabilization of kinetochore–microtubule (KT-MT) attachments. In the presence of unbalanced merotelic attachments, microtubules on the incorrect side would efficiently be destabilized. This model cannot explain the persistence of KT-MT attachments seen experimentally in permanent laggards at the spindle midzone (balanced merotelic attachments). Model 2: Midzone Aurora B activity promotes anaphase error correction of merotelic kinetochores by stabilizing KT-MT attachments, evidenced by the accumulation of marks such as pPlk1 (Thr210). This stabilization would assist in the mechanical transmission of spindle elongation forces to promote the correction of unbalanced merotelic attachments on transient lagging chromosomes. Balanced merotelic attachments would be expected to result in permanent laggards that remain attached with microtubules, in line with observations in living PtK1 cells and 3D electron microscopy reconstructions (i–iv; modified with permission from Salmon et al., 2005). Microtubules (magenta) and kinetochores (green) are depicted. White arrowheads indicate permanent or transient merotelic attachments. Scale bar is 5 μm.