Considering that LEN shares a capsid-binding site with multiple phenylalanine-glycine (FG)-motif-containing cellular cofactors essential for HIV replication, including those present in the cytoplasm (Sec24C), the nuclear pore (Nup153), and the nucleus (CPSF6), it is not unexpected that a portion of the evaluated binding site substitutions could also impair these and possibly other capsid-host interactions necessary for the productive infection of target cells (29, 34, –, 39, 60). The gene discussed is SEC24C; the disease is infection.