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Although generally accepted as indolent disorders, a considerable fraction of MPN patients exhibit progressive, and sometimes accelerated, bone marrow fibrosis, reflecting a critical shift toward a more debilitating condition marked by an increased symptom burden. As marrow scarring advances, hematopoietic capacity declines, severely compromising both patients' quality of life and survival. Increasing evidence highlights the crucial involvement of multiple players and mechanisms orchestrating marrow fibrotic transformation, thereby reflecting the multifaceted nature of this pathogenetic process. In this review, we untangle the pro\u2010fibrotic programs underlying fibrosis progression in MPN, critically analyzing the available scientific literature. We explore the potential impact of the mutational landscape on the fibrotic transformation risk and examine the role of dysfunctional megakaryocytes as principal catalysts of fibrotic remodeling. 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