MAP4K1 and neoplasm: In fact, Hernandez et al. had argued that the ability of the adoptive transferred catalytically-inactive K46E HPK1 mutant T cells to acquire an enhanced activated phenotype in vivo through priming by the host’s wild type dendritic cells suggests that disruption of HPK1-regulated kinase activity in T cells is sufficient to confer the enhanced tumor immunity phenotype independent of the contribution from enhanced antigen presentation by the kinase inactive K46E HPK1 dendritic cells (Hernandez et al., 2018).