As previous studies demonstrated that infection of humans with influenza A virus leads to an induction of apoptosis of a portion of CD3+, CD4+, CD8+, and CD19+ lymphocytes, thus resulting in a severe transient leukopenia, and that lymphocyte apoptosis, which represents a part of an overall beneficial immune response could be a possible mechanism of disease pathogenesis [4, 5]. The gene discussed is CD4; the disease is infection.