Interestingly, genomic silencing of DYRK2 increased the ability of cells from pulmonary metastases of breast cancers to form mammospheres during serial passage, an assay of self-renewal capacity, and this effect was associated with elevated KLF4 levels; however, in this case, KLF4 expression was regulated by the androgen receptor through a pathogenic DYRK2-AR-KLF4 pathway, although the mechanism by which DYRK2 activated the androgen receptor was not identified81. This evidence concerns the gene KLF4 and breast carcinoma.