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For decades, a critical question has persisted: is IMAT a passive biomarker of disease progression or an active pathogenic agent? This review synthesizes emerging evidence to address this question by exploring several key areas. We first evaluate the mechanisms by which IMAT impairs muscle function, examining evidence for its dual role as both a physical disruptor and a local source of unbalanced paracrine signals. By integrating findings from human studies with insights from diverse animal models, we also highlight significant translational challenges, particularly the resistance of common rodent models to developing human-like IMAT pathology. Furthermore, we review the cellular origin of IMAT to resident fibro\/adipogenic progenitors (FAPs), a highly plastic cell population that supports regeneration in healthy muscle but can differentiate into adipocytes under pathological conditions. We then dissect the complex signaling network that governs this fate switch\u2014specifically the balance between proadipogenic \u201ctriggers\u201d and inhibitory \u201cbrakes\u201d that becomes dysregulated in disease. The evidence increasingly points to IMAT as an active contributor to muscle decline. 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