Mastocytosis is one of the most common benign breast diseases, and its association with breast cancer has been of great interest to scholars. As early as the 1960s, many scholars have suggested the association of cystic hyperplasia with breast cancer through the results of coexistence studies and retrospective clinical investigations of paraneoplastic lesions. After the 1970s, a large number of clinical and epidemiological studies have confirmed the association of mammary hyperplasia with breast carcinogenesis after long-term follow-up studies of patients with biopsy-defined mammary hyperplasia, using the incidence of breast cancer in the general population as a control standard. The most important of these publications include Duppont and Page et al. 1985 in the New England Journal of Medicine, which published the results of more than 10,000 cases with a 17.5-year follow-up. Their conclusions clearly suggest that: (1) the following lesions have little chance of becoming cancerous, such as cystic disease, ductal dilatation, sclerosing adenopathy, sclerosis and fibroadenomatous changes; (2) biopsy findings of mild epithelial hyperplasia and sweat gland hyperplasia are not significant under 45 years of age; and (3) the incidence of atypical hyperplastic carcinoma of the breast increases 4.7-fold compared to controls, and if there is a family history of breast cancer, the incidence of breast cancer increases nearly 10-fold. Their findings confirmed the relationship between breast epithelial hyperplasia and atypical hyperplasia and breast cancer occurrence. Thereafter, it further classified cystic hyperplasia of the breast by histological type into cysts, sweat gland hyperplasia, adenopathy, sclerosing adenopathy, inflammation, calcification, intraductal papilloma, and/or epithelial hyperplasia by comparing women with different pathomorphological lesions defined by biopsy with women of the same age who did not have a breast biopsy, using the rate of development of invasive carcinoma of the breast at 10-20 years of follow-up as the risk level. The risk of breast cancer was not increased in non-proliferative lesions such as cysts, sweat gland hyperplasia, adenopathy, sclerosing adenopathy or inflammation; (2) those with ductal epithelial hyperplasia without atypical hyperplasia, including general, moderate or exuberant hyperplasia, had a mildly increased risk (1.5-2.0 times the risk of breast cancer in the control group); and (3) those with epithelial atypical hyperplasia, including ductal atypia and small epithelial hyperplasia. The risk of invasive carcinoma was highly increased (the risk of breast cancer was 8-10 times higher than that of the control group), while the risk of in situ carcinoma, including lobular carcinoma in situ and ductal carcinoma in situ, was highly increased (the risk of breast cancer was 8-10 times higher than that of the control group). This result further clarifies the significance of atypical hyperplasia in the carcinogenesis of benign breast diseases; its development process is normal breast epithelial cells → general proliferating epithelial cells → atypical proliferating epithelial cells → carcinoma in situ → invasive carcinoma. After repeated studies and arguments Page et al. classified breast proliferative lesions into 4 categories: A non-proliferative lesions, B general epithelial hyperplasia, C epithelial atypical hyperplasia, and D carcinoma in situ, to guide clinical treatment and follow-up monitoring. The follow-up period was 2-7 years from the first surgical detection of atypical epithelial hyperplasia to the second surgical pathology confirming the increase of atypical epithelial hyperplasia in the breast, and the interval between the detection of early breast cancer was 2-10 years. Preliminary studies on cellular ultrastructure, receptor status, proliferation characteristics, changes in oncogene products and expression of tumor-associated antigens in atypical hyperplasia of breast ductal epithelial cells suggest that atypical hyperplasia can, to a certain extent, represent the initiation and transition stages of carcinogenesis, and that the transformation of atypical hyperplasia of breast epithelium to cancer involves a series of recognizable processes. Research on the treatment of precancerous breast lesions also deserves attention. There are some effective methods for clinical diagnosis of early breast cancer, including mammography, color ultrasonography, mammography and ductoscopy, and breast MRI if available. However, there is no effective means to detect and monitor atypical hyperplasia. Clinical research should focus on the link between clinical manifestations and pathology of mastocytosis, and strengthen the research and monitoring of high-risk groups with possible precancerous lesions. Follow-up studies have found that the incidence of atypical hyperplasia is significantly higher in patients with limited thickening of the breast that does not change with the menstrual cycle and does not improve with systematic drug therapy, as well as in patients over 40 years of age with symptoms of breast hyperplasia, suggesting that clinical examination, biopsy and follow-up should be strengthened for this group of patients.