Although we have proposed that the rhMIF differential response in the PBMC from RA patients may be due to a higher expression of MIF receptors, we must also consider that the response observed between the study groups and the response to LPS could be due to a lower expression of the LPS receptor because it has been reported that different treatments in RA patients (chloroquine, methotrexate, and sulfasalazine) can affect the response to LPS through decreased mRNA expression of TLR4 [30,31,32,33], and this occurs possibly by inactivation of NF-κB [30]. This evidence concerns the gene NFKB1 and rheumatoid arthritis.