In contrast to experimental tumor models in mice, CMCs develop naturally, reproducing the same environmental and genetic aetiology as occurs in humans, grow in immunocompetent organisms [67] and share strong clinical (e.g. hormonal dependence, age of onset, histological appearance, prognostic factors, course of the disease) and molecular (e.g. tumor genetics, overexpression of steroid receptors, proliferation markers, EGF, p53 mutations, metalloproteinases, cyclooxygenases) similarities to human BC [20,22]. The gene discussed is EGF; the disease is neoplasm.