The spindle assembly checkpoint (SAC) ensures accurate chromosome segregation during mitosis, but its efficiency is highly variable during early embryonic development. Previous studies in Caenorhabditis elegans have shown that the SAC functions from fertilisation and have attributed the variation in SAC strength to differences in cell size and cell fate. Now, Stefania Castagnetti and colleagues employ the ascidian Phallusia mammillata to reveal the relationship between cell size, cell fate and SAC activity in chordates. They show that mitotic duration increases from the 8th cell cycle in the absence of spindle microtubules (i.e. in nocodazole-treated embryos) in a SAC-dependent manner. By imaging kinetochores, the authors determine that the SAC is inactive during initial cell cycles and only becomes functional at the 8th cell cycle, when the SAC response increases in both strength and variability during subsequent cell cycles. Alteration of the anterior-posterior patterning using overexpression and pole-ablation approaches shows that posterior-fated cells have weaker SAC activity than anterior ones. In addition, within cells of the same fate, the SAC response is stronger in smaller cells. Together, these data show that SAC components are not recruited to the kinetochore in early stages and SAC strength increases at each cleavage division in a lineage-specific manner.