Key pathways, including NF-κB, IL-6/STAT3, AMPK, and PGC-1α, are discussed in detail in Section 2.1; here, we focus on additional mechanistic aspects such as the IL-6/STAT3–SOCS3 axis, the activation of the ubiquitin–proteasome system (UPS) and the autophagy–lysosome pathway, and the role of tumor-derived extracellular vesicles (EVs) in propagating catabolism. The gene discussed is IL6; the disease is neoplasm.