SOAT1 and Cachexia: Research has demonstrated that IFN-γ promotes the upregulation of muscle-specific E3 ubiquitin ligases, such as MuRF1 and Atrogin-1, by activating the JAK/STAT signaling pathway, which accelerates protein degradation.399 The elevation of IFN-γ is closely associated with the release of proinflammatory signaling molecules (such as TNF-α and IL-6), which collectively enhance systemic inflammatory responses and worsen the symptoms of cachexia.