This is supported by recent observations, such as Cdk1 activity impaired by the absence of Fez1/Lzts1 predisposes mice to cancer development [38], inhibition of Cdk1 mediates protection from apoptosis in Cdc20-depleted cells [39], a low ratio of CDK2 to CDK1 activity is associated with a favorable prognosis in breast cancer patients [40], phosphorylation of p62 by Cdk1 is necessary to restrain tumorigenesis in vivo in response to Ras-induced transformation [41], and CDK1 inhibits cancer cell migration and invasion by phosphorylation of EZH2 at Thr 487 [42]. This evidence concerns the gene FEZ1 and breast cancer.