Interestingly, its upstream regulator, miR-30e-5p, switched from being downregulated in the early transition (MCF10A.P to MCF10.AT1) to upregulated in this mid transition (MCF10.AT1 to MCF10.DCIS); its upregulation could lead to inhibition of CPSF6, a gene modulator of translation, and eventually cause a decrease in translation. This evidence concerns the gene CPSF6 and ductal breast carcinoma in situ.