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The review delves into the complexities of TGF-β signaling in keloids, emphasizing the significance of both Smad-dependent and Smad-independent pathways. While the classical Smad pathway has been extensively studied, recent findings underscore the critical roles of alternative pathways like MAPK, PI3K/Akt, and others in keloid pathogenesis. These non-Smad pathways contribute to fibroblast proliferation, migration, and chronic inflammation, suggesting potential targets for more effective therapies. The document highlights the intricate crosstalk between these pathways and TGF-β signaling, which creates a self-sustaining fibrotic environment, making keloids resistant to treatment. It suggests that targeting these pathways could disrupt the fibrotic cascade and improve therapeutic outcomes, with precision therapies potentially reprogramming the fibrotic microenvironment to address high recurrence rates of traditional treatments.