In summary, as schematically illustrated in Figure 5C, the proposed mechanism for tasquinimod's potency involves EPR facilitated delivery of albumin bound drug via leaky vessels into the tumor microenvironment lacking lymphatic drainage and the resulting uptake of free compound into myeloid, endothelial and tumor cells inhibiting HDAC4/S100A9 signaling uniquely activated and required for survival and growth within the cancer, but not in normal, tissue microenvironment. This evidence concerns the gene S100A9 and neoplasm.