Both the chemotherapeutic treatment and the tumour itself promote the release of proinflammatory cytokines, such as tumour necrosis factor alpha (TNF-α), tumour necrosis factor-like weak inducer of apoptosis (TWEAK), interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-8 (IL-8), and intracellular interferon gamma (INFγ), that promote the activation of NF-κB transcription factor, a regulator of gene expressions associated with skeletal muscle degradation [52,53,54]. This evidence concerns the gene IL6 and neoplasm.