To directly estimate the cytotoxicity of TLR3 signaling in primary AML blasts and obtain insights in the underlying mechanisms, we nest stimulated CD33+ cells isolated from 8 AML patients of Study Cohort 1 with the TLR3 agonist polyI:C in the optional presence of an IFNAR1-blocking antibody. Here, IFNAR1 is linked to acute myeloid leukemia.