These depletion studies indicate that IT IL-12 therapy-mediated tumor immunity is mediated, in large part by CD8+ T cells, and suggest that IT IL-12 treatment may function as an in situ vaccine through the induction of cell death-mediated antigen release in a pro-inflammatory, strongly Th1-biased tumor microenvironment (TME) [15]. This evidence concerns the gene CD8A and neoplasm.