Other potential targets include NPM1 (reports suggesting a role for ATRA in NPM1 mutated diploid AML), c-KIT in CBF leukemias, the JAK-STAT signaling pathway in post-MPN AML, the MAPK pathway in RAS mutated leukemias and various cellular signaling components which include a number of tyrosine and serine/threonine kinases. This evidence concerns the gene CEBPZ and acute myeloid leukemia.