Ertych, Stolz et al. found an increase in microtubule assembly rates in colorectal cancer cells, and reducing microtubule assembly to the rate of normal cells suppressed chromosomal instability (CIN). The increased microtubule assembly rates were associated with transient spindle geometry defects and promoted lagging chromosomes. Additionally, CHK2–BRCA1 negatively regulated aurora kinase A (AURKA) to modulate microtubule assembly rates, and CHK2 loss or AURKA overexpression frequently occurred in colorectal cancer samples. Unexpectedly, they found that restoring microtubule assembly rates to normal in colorectal cancer cells increased their growth in soft agar and as xenografts in vivo, even though the suppression of CIN was maintained.