To further ensure that R10015 blocks HIV by inhibiting LIMK, we performed a series of experiments demonstrating that (i) R10015 strongly blocked cofilin phosphorylation, whereas the other upstream kinases were largely unaffected, demonstrating its good selectivity (Fig. 3D); (ii) R10015 effectively blocked actin polymerization and T cell chemotaxis (Fig. 3F and G), as these are the expected properties of LIMK inhibitors; and (iii) most importantly, R10015 selectively blocked wild-type HIV infection, but not VSV G-pseudotyped HIV infection, when used early during viral entry (Fig. 4). The gene discussed is CFL1; the disease is HIV infectious disease.