TP53 and neoplasm: Utilizing a lineage‐traced mouse model, that study unequivocally showed that polyploidization, in a deterministic manner, emerged as a mechanism to mitigate significant chromosomal losses accrued following the loss of p53 and then acquiring further gains and amplifications, thus fueling tumor progression.[28] By generating and buffering aneuploidy, polyploidization can contribute to further adaptive events, such as therapeutic resistance.[29]