Different mechanisms have been postulated for the relation between tumor and CRP: (a) CRP could be released in response to the inflammatory status caused by the tumor growth, (b) CRP could be a result of the body’s response to tumor antigens or the increased production of inflammatory cells from the malignant cells [12], or (c) CRP release is mediated through its precursor IL-6 which has been shown to be upregulated in response to treatment, e.g., paclitaxel and platinum drugs and involved in cancer resistance [45]. This evidence concerns the gene CRP and neoplasm.