NFATC1 and acute myeloid leukemia: Development of this mouse model was prompted by our recent observations showing that many FLT3ITD-positive and -negative AML patients frequently overexpress NFATC1. We have also shown previously in a murine model of inflammation-driven pancreatic cancerogenesis that NFATC1 is a relay switch converting KrasG12D-driven pre-neoplastic changes into a rapidly lethal metastatic pancreatic cancer [7].