To determine the mechanistic role of specific miRs in the dysregulation of DNMT3b among breast cancer cell lines, the complementary approach of modulating miR levels by transfection of pre-miR precursors (to enforce miR expression in cells lacking a given miR) or transfection of antagomirs (to knockdown miR expression in cells that express normal levels of a given miR) was employed. The gene discussed is DNMT3B; the disease is breast carcinoma.