There is evidence to show that genetic defects in innate immune functions like toll-like receptor (TLR) 4, interleukin15, TLR3, TLR10, etc., as well low numbers of CD19, CD56 and/or CD4 cells, are common in patients with CPA: they are therefore risk/predisposing factors for CPA [21,36,37,38]. The gene discussed is CD19; the disease is congenital primary aphakia.