To determine which of these were required for IFNβ-mediated up-regulation of CD38 expression, primary AML apheresis samples were pre-treated with inhibitors for Jak 1/2 (Ruxolitinib, targeting the JAK/STAT canonical pathway), p38 (SB202190, targeting the non-canonical p38 MAPK pathway) and MEK (PD0325901, targeting Erk). This evidence concerns the gene SOAT1 and acute myeloid leukemia.