TGFβ3 is thought to facilitate a scar-free fibrosis response, unlike TGFβ1 and TGFβ2, and depending on the context can mediate an anti-inflammatory response, with high levels of TGFβ3 correlating with reduced autoimmune encephalomyelitis in a mouse model13, or pro-inflammatory state, as lung fibroblasts can produce a pre-metastatic niche in response to TGFβ3 expressed by breast cancer cells4. This evidence concerns the gene TGFB1 and neoplasm.