As Castiblanco and colleagues [93] recently articulated, the differences in allele and genotype frequencies of diverse human populations depend upon their evolutionary and epidemiological history, including environmental exposures, which might explain why some risk alleles to autoimmunity may be protective factors to infectious diseases and vice versa in a given population (e.g., PTPN22 [94, 95] and TNF [96]). This evidence concerns the gene PTPN22 and infectious disease.