Desmoid tumor (DT) is a rare clinical tumor, accounting for 0.03% of soft tissue tumors, and was first named by Muller in 1838. According to its growth site, it can be divided into abdominal wall and extra-abdominal wall, and the latter was first reported by Nichols (1923). Extra-abdominal wall DT is less common than abdominal wall DT. Sclerofibromas are more common in women, especially abdominal wall DT, and occur more often in women of childbearing age. Thus, it is generally believed that the occurrence of hard fibroids is related to endocrine hormones, and estrogen has been experimentally demonstrated to induce fibroid formation in animals. Genetic factors have also been shown to be closely related to the disease, with the incidence of familial adenomatous polyposis ranging from 8% to 38%, 852 times higher than that of the general population. Trauma has been reported to be associated with the development of this disease. Sclerofibrosarcoma presents clinically as a slow-growing solid tumor with symptoms related to the location of the tumor. When the tumor is small, it is asymptomatic. When the tumor enlarges and compresses the adjacent tissues and organs, it may cause pain, numbness and discomfort, and even organ dysfunction. Clinical examination and imaging examination (ultrasound, CT and MRI) have reference value for diagnosis, but their main function is to understand the location of tumor and its relationship with neighboring tissues and organs, so as to provide help for treatment. It mainly relies on pathological examination for clear diagnosis. Its histological manifestations are interwoven fibroblasts and myofibroblasts into bundles, and fibroblasts often invade adjacent normal structures, surrounded by a large amount of collagen matrix, in which the number of cells is high. It is distinguished from malignant fibrosarcoma by the lack of nuclear and cytoplasmic manifestations of malignant tumors, especially the absence of nuclear division phase. Sclerofibrosarcoma does not usually metastasize, but repeated reissue surgeries may lead to metastasis of the tumor. The disease is aggressive in growth and is prone to recurrence with a recurrence rate of 25% to 40%. Therefore, the disease is generally considered to be a low-grade malignant tumor. Treatment is mainly surgical. Because of the aggressive growth and easy recurrence of the disease, extended resection should be performed as far as possible, but the scope of resection and the significance of histological examination of the resection margin are still controversial. Generally, the resection margin should be at least 2-3 cm away from the tumor. After cutting down the specimen, the specimen should be observed visually whether the resection margin is normal tissue, if white hard tissue is found, it means that the resection margin is not clean and the resection scope should be expanded; if it cannot be determined, frozen pathological examination should be performed, and the examination of the surgical resection margin should be emphasized. The literature reports that the recurrence rate of those with no tumor at the cut edge by pathological examination is only 4%. For the tissue defects caused by extended surgery, alternative materials and skin-muscle flap repair can be used. For example, peritoneal defects can be replaced by broad fascia, nylon, taping cloth, polypropylene, etc. For larger tumors or multiple recurrences that cannot be surgically eradicated, radiotherapy was once thought to be effective. It has also been suggested that adjuvant radiotherapy can achieve better local control rates. For example, Kiel believes that radiotherapy is more effective in cases with extensive lesions that cannot be cured by surgery, as well as with small marginal recurrences, and he reported that in 25 cases of radiation therapy, 76% were in partial or complete remission and 59% were cured. The dose of radiotherapy is generally 50-60 Gy. However, there are many reports that fail to support the effectiveness of radiotherapy. Drug therapy is effective for this disease. The drugs reported to be applied to this disease are adriamycin, actinomycin D and vincristine, and another class of therapeutic drugs is cyclic adenosine? phosphate (CAMP) modulators, non-steroidal anti-inflammatory drugs (NSAIDs) and anti-endocrine agents. Since the occurrence of this disease is closely related to estrogen, the use of triamcinolone acetonide has been reported abroad to be effective in the treatment of this disease.