They are proficient in inducing CD4+ T helper cell polarization but they are also capable of efficiently presenting soluble but also immune complexed antigens to CD8+ T cells.43 57 In a tumor regression model, CD11b+ cDC2 that displayed an IFN-stimulated gene expression (ISG+ DC) could present intact tumor-peptide-MHC-I complexes via cross-dressing.58 As we observed an upregulation of several genes involved in type I IFN signaling during BRAFi-sensitive phase, we assume that the CD64+ cDC2 population we identified resemble this inflammation-induced DC subtype. The gene discussed is IFNA1; the disease is neoplasm.