Unlike epithelial malignancies, there is no basement membrane to clearly distinguish pre-neoplastic dysplastic change, in situ carcinoma from frankly malignant invasive carcinomas. Instead, between benign mesenchymal tumors and frankly malignant sarcomas, there exist two dozens of tumor entities, which are commonly characterized by locally aggressive behavior but can be divided into non-metastasizing and rarely metastasizing subgroups. For the latter, the metastatic rate is defined as < 2%, but you are unable to predict which single case will do so beforehand based on histological analysis. Actually, even assignment of benignancy in mesenchymal neoplasms is by no means equivalent to “never metastatic” but just extremely rare, with the actuarial metastatic rate of benign mesenchymal tumors being estimated to be < 1 per 50 thousands. There are several unique characters of indolent soft tissue tumors, including (1) the discrepancies between classification, either between WHO and International classification of disease for oncology (ICD-O) and between bone and soft tissue for the morphologically identical tumors by WHO, (2) the majority of cases belonging to the adipocytic, fibroblastic/myofibroblastic, or fibrohistiocytic tumor categories, (3) tumor depth-dependent nomenclature for histologically identical tumors, and (4) overrepresentation of tumors of uncertain differentiation or with specific gene alterations, such as mutation, amplification, gene fusion, or much rarely, deletion. To fit the main theme of today’s symposium, I cannot go over each entity but focus on some representative tumors, including desmoid-type fibromatosis, diffuse-type tenosynvoial giant cell tumor (DT-TSGCT), inflammatory myofibroblastic tumor (IMT), and dermatofibrosarcoma protuberans (DFSP), to highlight their clincopathological features, pathogenetic mechanisms, critical diagnostic differentials, incidence and features of frankly sarcomatous transformation. Of these, desmoid-type fibromatosis never undergoes sarcomatous change unless radiation therapy is administered. However, DT-TSGCT, IMT, and DFSP are gene fusion-driven and may spontaneously present with or secondarily develop frankly sarcomatous histology at very variable levels of risk but have available targeted therapies when accurate diagnosis is made. For instance, imatinib has been shown to effectively inhibit DT-TSGCT and DFSP, whiles IMT is responsive to crizotinib.