CCND1 and breast neoplasm: The mechanism by which SIX1 promoted breast tumor formation may be reinstating its properties normally displayed in early developmental tissues, including stimulation of proliferation and inhibition of apoptosis.[49] SIX1 transcriptionally induces the expression of growth-promoting genes, such as cyclin A1, cyclin D1, and c-Myc.[50,51] By increasing these gene expression, SIX1 promoted malignant transformation.[17,18]