Chen et al. also reported that cyclin E overexpression, which increased replication stress, sensitizes triple-negative breast cancer to WEE1 inhibition (37); a more recent study demonstrated that the amplification of CCNE1, which encodes cyclin E, is synthetically lethal with PKMYT1 kinase inhibition, a functionally redundant kinase of WEE1, emphasizing that the G2/M checkpoint is a critical vulnerability in cancers with high replication stress (38). This evidence concerns the gene CCNE1 and triple-negative breast carcinoma.