Stress‐induced HSP‐peptide complexes (commonly induced during apoptosis) are more efficiently taken up via scavenger receptors and TLR on the DCs surface, and they induce efficient cross‐priming and skewing of the immune response toward a TH1‐type profile.[204] In vitro, human DCs loaded with melanoma cells that were heat‐treated at 42 °C before being killed showed more efficient cross‐priming against naïve human CD8+ T cells than DCs loaded with unheated melanoma cells. This evidence concerns the gene CD8A and melanoma.