Additionally, the overexpression of FOXM1 prevents the phosphorylation of YAP1 and subsequently upregulates YAP1 expression, therefore promoting cancer cell proliferation, migration, and stemness [73], N Yang et al. reported that there exists a positive feedback between nuclear aurora kinase A (AUPKA) and FOXM1 in BCSCs, which is essential for the maintenance and self-renewal of BCSCs [74], Specifically, AURKA, as a transactivating co-factor, transcriptionally activates FOXM1 expression independent of its kinase activity. The gene discussed is YAP1; the disease is cancer.