Although proteomic profiling with the small panel studied was unable to detect differences between staphylococcal vs. non-staphylococcal PJI, or between aseptic loosening, instability, stiffness, osteolysis, or other causes of NIAF, two proteins were differentially expressed when comparing causative species of PJI, with elevated IL-17A in S. aureus compared to S. epidermidis and Staphylococcus lugdunensis-associated PJI, and elevated CCL11 in S. epidermidis compared to S. aureus and Streptococcus agalactiae-associated PJI [216]. This evidence concerns the gene IL17A and juvenile polyposis syndrome.