Cleavage failure, an intractable mitotic defect, is thought to be dangerous to the organism because it immediately produces centrosome amplification.   If the binucleate cell enters another mitosis, consequent spindle multipolarity can lead to genomic instability and genetic imbalances that can drive the evolution of unregulated growth characteristics.   We re-examined the basis for the attractive and increasingly accepted proposal that normal mammalian cells have a tetraploidy checkpoint that arrests binucleate cells in G1 thereby preventing their propagation. Using cytochalasin at the concentration previously employed to block cleavage, we confirm that most binucleate cells arrest in G1.   However, when we use lower concentrations of cytochalasin, binucleate cells undergo DNA synthesis and later proceed through mitosis in >80% of the cases for the hTERT-RPE1 human cell line, primary human fibroblasts, and the REF52 cell line previously used to establish the existence of this checkpoint.   These observations provide a functional demonstration that the tetraploidy checkpoint does not exist in normal mammalian somatic cells.