This is not surprising as many reasons can explain this scenario: (1) The activation of humoral immunity can be associated with other conditions, not necessarily with CHIP; (2) Different CHIP mutations in immune cells can have divergent effects on the inflammation; (3) Even in the case of mutations promoting inflammation, their effect on CAVD pathogenesis depends on several other exogenous or endogenous individual factors; (4) Some patients with CHIP may not have been recognized as they may be carriers of CHIP mutations on genes not tested in this study. This evidence concerns the gene STUB1 and congenital bilateral aplasia of vas deferens from CFTR mutation.