Fibrosis is not a unidirectional, linear process, but a dynamic one resulting from an interplay of fibrogenesis and fibrolysis depending on the extent and severity of a biologic insult, or lack thereof. Regression of fibrosis has been documented best in patients treated with phlebotomies for hemochromatosis, and after successful suppression and eradication of chronic hepatitis B and C infections. This evidence mandates a reconsideration of the term “cirrhosis,” which implies an inevitable progression towards liver failure. Furthermore, it also necessitates a staging system that acknowledges the bidirectional nature of evolution of fibrosis, and has the ability to predict if the disease process is progressing or regressing. The Beijing classification attempts to fill this gap in contemporary practice. It is based on microscopic features termed “the hepatic repair complex,” defined originally by Wanless and colleagues. The elements of the hepatic repair complex represent the 3 processes of fragmentation and regression of scar, vascular remodeling (resolution), and parenchymal regeneration. However, regression of fibrosis does not imply resolution of cirrhosis, which is more than just a stage of fibrosis. So far, there is little to no evidence to suggest that large regions of parenchymal extinction can be repopulated by regenerating hepatocytes. Similarly, the vascular lesions of cirrhosis persist, and there is no evidence of complete return to normal microcirculation in cirrhotic livers. In addition, the risk of hepatocellular carcinoma is higher compared with the general population and these patients need continued screening and surveillance.

Hepatic angiomyolipoma (HAML) is a rare mesenchymal neoplasm that belongs to the perivascular epithelioid tumor family. Though it is characteristically, a triphasic tumor composed of smooth muscle, blood vessels, and adipocytes, the smooth muscle cells are often epithelioid and can represent the near‐entirety of the tumor. A HAML composed predominantly of epithelioid smooth muscle cells occurring in the liver presents significant diagnostic challenges as many liver tumors are composed of large epithelioid cells. Furthermore, even if the tumor is not composed predominantly of epithelioid smooth muscle cells, this may be the only component present in a fine‐needle aspiration (FNA) or core needle biopsy. A 38‐year‐old female with a 3 month history of abdominal pain, nausea, and diarrhea was found to have a 12 cm right hepatic lobe mass. FNA biopsy revealed a moderately cellular specimen composed of plump epithelioid cells with indistinct cell borders, low N:C ratio, round to oval nuclei, fine chromatin, occasional nucleoli, and abundant vacuolated to fibrillary cytoplasm. Rare intranuclear inclusions and occasional foamy macrophages were noted. Concurrent core biopsy revealed large polygonal cells with eccentric nuclei and clear, vacuolated to granular, eosinophilic cytoplasm that stained strongly for HMB45, confirming the diagnosis of HAML. Because HAML is a rare tumor, this diagnosis can be easily overlooked; cognizance of the typical cytologic, histologic, and immunophenotypic findings is crucial to establishing a diagnosis.

Solitary fibrous tumor (SFT) is an uncommon fibroblastic neoplasm that is most commonly associated with the pleura but has also been reported in almost all anatomic sites. Although the majority of SFTs are benign, few cases follow a malignant clinical course and may recur and/or metastasize after several years of their original occurrence. Only 16 cases of pancreatic SFTs are reported so far, and only one has metastasized to lung and subcutis. Pancreatic SFT resembles more common neuroendocrine tumor and gastrointestinal stromal tumor (GIST) radiographically and is at times almost indistinguishable from GIST histologically. Diagnosis of SFTs particularly, if attempted on biopsied specimens, can be very challenging due to its rare occurrence and nondescript morphology. It is imperative to understand the pathological spectrum of this entity to avoid misdiagnosis. We report a case of pancreatic SFT in a 43-year-old male with some unusual morphologic and immunohistochemical features including pseudoangiomatous growth pattern, a hypercellular area demonstrating nuclear pleomorphism, and only focal positivity for cluster of differentiation (CD)34. These atypical features can pose even more diagnostic challenge by causing additional confusion with other malignancies like dedifferentiated liposarcoma and vascular tumors. The potential diagnostic pitfalls are discussed.