In contrast to mice crossed to CD4-Cre animals, pTαSHP2mut mice did not develop splenomegaly and cell numbers were comparable to those isolated from control mice indicating that the development of JMML-like features is rather the result of the gain-of-function mutation in myeloid cells than the result of a T cell intrinsic mechanism (Figures 1A, B). Here, CD4 is linked to juvenile myelomonocytic leukemia.