Immune- or tumor cell-derived pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor α (TNFα), high mobility group 1 (HMGB-1) [5] or IL-1β [6], trigger muscle wasting by inducing the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), Janus kinase/signal transducers and activators of transcription 3 (JAK/STAT3) or Forkhead box-containing subfamily O3 (FoxO3) pathways [7,8,9,10]. Here, STAT3 is linked to neoplasm.