Differential tumor cell sensitivity and their immune microenvironment (e.g. higher levels of myeloid CD11b+ cells in LLC-OVA, which may hamper immune stimulating therapies (42, 43), or the higher lymphocytic infiltrate in B16-OVA, suggestive of a less hostile environment for lymphocyte infiltration) may account for these differences. This evidence concerns the gene ITGAM and neoplasm.