Evidence suggests that DCIS-associated MECs fail to polarize luminal epithelial cells.148 Discordant markers have been identified between normal and DCIS-associated MECs on immunohistochemical analysis; these include P63, calponin, CD10, and αvβ6 integrin.147,149–152 Notably, Ding et al. found that the functions of normal MECs are partly maintained via an interactive network involving p63 and TCF7 which accomplished by regulation of extracellular matrix proteins and cell adhesion. This evidence concerns the gene MME and ductal breast carcinoma in situ.