The reduction of the interleukin-correlated T-cell kinase, which can stimulate T-helper cell type 1 CD4 T-cell growth, provoking a decrease of infections, or a restoration of the humoral immunity with an increased production of immunoglobulin A. However, the real reason of an improvement in immunoglobulin function after prolonged treatment remains unidentified (170). The gene discussed is CD4; the disease is infection.