“…9,10 In fact, the majority of previous studies have shown that alteration in the host defensive cell functions, immunological and immunogenetic characteristics, such as neutrophil and lymphocyte dysfunctions, aberrant cytokine production and specific HLA types, are associated with the pathogenesis of some, but not all, EOP patients. 5,[11][12][13][14][15] Previous studies showing a high prevalence of EOP in certain families, [16][17][18][19] twin studies, 20 and the linkage with specific HLA types [21][22][23] suggest that susceptibility to this disease is heritable and that certain genetic risk factors may be involved. 24 Therefore, we have hypothesized that the heterogeneous nature of EOP could be explained from various host risk factors.…”