However, other mechanisms, such as DDR aberrations, nucleotide starvation, replicative stress, and, as more recently found, loss of the ATRX chromatin remodeler gene [36] and low phosphatase and tensin homolog (PTEN) expression [37], contribute to sensitize cancer cells to WEE1 inhibition, which, thus, proved monotherapy activity even in TP53-wild-type cancer cells [29,30,38]. This evidence concerns the gene WEE1 and cancer.