Although bispecifics like AMV564 (which targets CD33 on AML blasts) together with T cells can directly mediate killing of AML via a MHC independent mechanism, activation of T cells by bispecifics after target engagement can also enhance MHC-dependent killing of AML cells via local release of interferon gamma and subsequent upregulation of MHC class II on AML blasts [12]. The gene discussed is HLA-C; the disease is acute myeloid leukemia.