This indicates that, although TNF-α and IL-6 are well-accepted drivers of cachexia in disease (66, 67), our observations may be explained by the regulatory effect of PPS on NF-κB resulting in the downregulation of these cytokines, and further studies examining the transcriptional profile of cachexia-associated pathways may shed light on how PPS treatment ameliorates cachexia in PR8-infected mice. The gene discussed is NFKB1; the disease is Cachexia.