Nevertheless, the apparent opposing roles played by TET3 in AML, as demonstrated by simultaneous deletion of Tet2 and Tet3 in HSPCs in mice and shRNA knockdown or TET inhibitor treatment in human AML cells, are not explained by differences between the human and mouse diseases because TET3 inhibition also represses the growth of murine AML cells. Here, TET3 is linked to acute myeloid leukemia.