Given that some reports in rodents have described that TWEAK signaling can contribute to increase the clinical severity of autoimmune/inflammatory diseases such as RA, SLE or MS (7, 8), we decided to study TWEAK transcription in a proliferative/inflammatory condition such as that produced by the parasite Tetracapsuloides bryosalmonae during PKD. This evidence concerns the gene TNFSF12 and myeloid sarcoma.