Antiretroviral (ARV) therapy suppresses HIV, but viral replication rebounds once treatment is discontinued. The redistribution of lipids in the plasma membrane to form microdomains is crucial for viral entry and biogenesis during HIV infection. Researchers at Johns Hopkins University School of Medicine found neutral sphingomyelinase 2 (nSMase2) to be a key component of the late stages of HIV viral assembly and maturation; they hypothesized that nSMase2 inhibitors could help avoid viral rebound.