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The answer lies in the difference between central and peripheral effects

In rodent models of varicocele, histological changes include degeneration of the spermatogenic epithelium, disruption of seminiferous tubule architecture, inflammatory-cell infiltration, and increased oxidative stress within the testicular tissue ( The causal involvement of TNF- signaling in this inflammatory cascade has been further supported by gene-knockout evidence ( A theoretical hypothesis proposes that pre-activated immune cells may preferentially home to tissues vulnerable to microcirculatory disturbances, such as erectile tissue ( Animal model studies have demonstrated that induction of varicocele is associated with increased immune cell infiltration in both the testis and the corpus cavernosum ( In summary, the activation and migration of immune cells in response to inflammatory stimuli within the testicular microenvironment play a critical role in the pathogenesis of conditions such as erectile dysfunction and spermatogenic impairment

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When independent researchers went looking for the gene that would build it in the human genome, in gut bacteria they could not find it

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