Our experiment, where we could restore sensitivity towards AC220 by PDP1 knockdown in primary patient AML blasts ex vivo, also points to the possibility that we may describe a real-world clinically relevant mechanism of secondary resistance towards FLT3 inhibitors, a phenomenon which occurs almost uniformly after weeks to months of monotherapy with these drugs [9, 10]. Here, FLT3 is linked to acute myeloid leukemia.