The latter showed that escape from accelerated senescence in both a p53-null non small cell lung cancer cell-line (NSCLC) in vitro and in primary tumours is due to overexpression of cdk1 [53] and survivin [54] and that aberrant expression of cdk1 promotes the formation of polyploid senescent cells, which are an important intermediary through which escape preferentially occurs [55]. The gene discussed is TP53; the disease is neoplasm.