Both genetic and acquired defects in the production of interleukin (IL-10), IL-12, IL-17, interferon–gamma (IFN-γ), mannose-binding lectin (MBL), toll-like receptors (TLR), and transforming growth factor–beta (TGF-β) have been implicated in CPA [18]. Here, TGFB1 is linked to congenital primary aphakia.