The fact that silencing of gelsolin expression does not completely inhibit HIV infection could be due to the existence of cells where siRNA-GSN oligos did not correctly silenced endogenous gelsolin, as observed in cells from new Figure 6C or D, or to the presence of other actin-associated proteins or adaptors, such as moesin and filamin-A [6,7], which could compensate the negative effect of gelsolin knockdown. Here, GSN is linked to HIV infectious disease.