Given that the HPK1-/- BMDCs were resistant to LPS-mediated activation-induced apoptosis and HPK1-/- T cells are also resistant to PGE2-induced apoptosis (Alzabin et al., 2009; Alzabin et al., 2010), it is possible that the potent anti-cancer immunity induced by tumor-pulsed HPK1-/- BMDCs is due in part to their ability to resist apoptosis induction by death receptor ligands or apoptosis-inducing factors present in the tumor microenvironment (TME) (Alzabin et al., 2009). This evidence concerns the gene MAP4K1 and neoplasm.