Similar results were observed through the inhibition of STAT3 signaling in C2C12 cells in vitro.359 Similarly, the administration of IL-6 receptor antibodies to C26 cachexia mice mitigated muscle loss.420 Hashimoto et al. demonstrated that recombinant IL-6 treatment reduced the diameter of C2C12 myotubes while increasing STAT3 phosphorylation and Atrogin-1 transcription.421 Overall, IL-6 phosphorylates STAT3 via the JAK/STAT pathway, leading to the overexpression of MAFbx and subsequent muscle wasting. Here, SOAT1 is linked to Cachexia.