However, the observation that depleting CD8 T cells did not rescue the melanoma growth in Colec11–/– mice (Supplemental Figure 6) suggests that regulation of antitumor immune responses by CL-11 may not be the primary mechanism for CL-11–dependent tumor growth, further supporting the notion that CL-11–mediated tumor cell proliferation is the primary mechanism for CL-11–dependent tumor growth. This evidence concerns the gene CD8A and melanoma.