Further, the CRP effect on atherosclerosis did not depend on PC binding as, when mutant proteins were constructed to lose PC binding activity (i.e., F66A/T76Y/E81A), “CRP” still bound atherogenic LDLs and, when injected into atherogenic-prone mice, slowed disease progression, and reduced the size of aortic lesions (94). The gene discussed is CRP; the disease is atherosclerosis.