Consistent with this possibility, in a syngeneic mouse model with BRAFi-resistant melanoma cells, which exhibited a similar modulation of AR expression and activity as the human cells, suppression of tumorigenicity by AR inhibitors was accompanied by increased infiltration and clusters of granzyme-positive CD8 T cells with adjoined areas of apoptotic (caspase 3-positive) tumor cells. The gene discussed is CD8A; the disease is neoplasm.