Taking into account the functions of these genes, their hypomethylation and potential activation may aid to promote cell death by apoptosis (DNASE1)50, induce degradation and turnover of mitochondria to facilitate necessary cell turnover (FUNDC2), and convert estrogen sulfates into free estrogens to protect from breast cancer resistance protein (BCRP)-mediated drug resistance (IDS)68 during ADH and DCIS stages. This evidence concerns the gene FUNDC2 and ductal breast carcinoma in situ.