In an athymic mouse tumor xenograft model where tumors were formed using immortalized murine embryonic fibroblasts (MEFs) overexpressing Bcl-xl, DNA alkylating therapy led to inhibition of protumor cytokines such as IL-4, IL-10, and IL-13, recruitment of innate immune cells including neutrophils, NK cells and macrophages into the treated tumor tissue and to complete tumor regression; loss of HMGB1 resulted in increased levels of protumor cytokines upon treatment and failure to activate innate immunity (79). The gene discussed is BCL2L1; the disease is neoplasm.