SOAT1 and bacterial infectious disease: Although the biochemical mechanisms by which SOCS2 alters the host’s response remain unknown, the fact that SOCS2 is known to play a key role in the negative feed-back of the cytokine-meditated response via JAK/STAT signalling pathways, supports the idea that our Socs2-deficient sheep fail to control the inflammatory process in response to intramammary bacterial infection, leading to impaired resistance to the disease.