Early parity is associated with a pronounced decrease in the risk of breast cancer, and additional live births reduce the risk even move. The protection afforded by early full-term pregnancy in women can be explained by the higher degree of differentiation of the mammary gland, which eliminates type 1 stem cells and creates a second type of stem cell (stem cell 2) that is able to metabolize carcinogens and repair DNA damage more efficiently than cells of the nulliparous breast. All though differentiation significantly reduces cell proliferation in the mammary gland, the epithelium remains capable of responding to a given stimulus, such as a new pregnancy. Under these circumstances, the cells that are stimulated to proliferate are derived from structures that have already been primed by the first cycle of differentiation. However, if the shift from stem cell 1 to stem cell 2 has not been completed, a sufficiently powerful carcinogenic stimulus may overburden the system, and successfully initiate a neoplastic process. Incomplete differentiation of this type may explain the development of breast cancer after a late first full-term pregnancy. The finding that differentiation is a powerful inhibitor of cancer initiation provides a strong rationale for pursuing the identification of the genes that control this process.