While we continue to explore the influence of melanoma‐derived factors on both T cells and APC populations, we do favor the hypothesis that incomplete differentiation arises from suboptimal T cell stimulation rather than direct T cell suppression, as this idea is consistent with previous work showing that CD8+ T cells do differentiate into functional effectors in B16‐involved LN when they are stimulated by exogenous, CD40L‐activated bone marrow‐derived dendritic cells (BMDC) [14] or when IL‐12 is administered to support T cell responses to tumor‐derived Ag [17]. The gene discussed is CD8A; the disease is neoplasm.