When SMs kill cells as single agents, as in AML cells, they do so via a two-pronged mechanism, simultaneously promoting TNF production and sensitizing to TNF- and RIPK1-dependent cell death (Varfolomeev et al., 2007, Vince et al., 2007, Wang et al., 2008, Wong et al., 2010). This evidence concerns the gene RIPK1 and acute myeloid leukemia.