Here, SHP-1 binds directly to a tyrosine residue (at position 429) on EpoR and removes phosphate groups from the receptor-associated JAK2.[36] The ability of SHP-1 to negatively regulate the JAK-STAT pathway has also been seen in experiments using mice lacking SHP-1.[37] These mice experience characteristics of autoimmune diseases and show high levels of cell proliferation, which are typical characteristics of an abnormally high level of JAK-STAT signalling.[37] Additionally, adding methyl groups to the SHP-1 gene (which reduces the amount of SHP-1 produced) has been linked to lymphoma (a type of blood cancer) .[38]