Although antiretroviral treatment (ART) blocks HIV replication, persistently infected cells form a latent reservoir, leading to rebound viraemia if treatment is interrupted. It has previously been reported that individuals who received allogeneic haematopoietic stem cell transplantation (allo-HSCT) from donors who lack CCR5, the main viral co-receptor, have been cured, as the virus remained undetectable even after ART was interrupted. By contrast, viral rebound has been reported in individuals who received allo-HSCT from donors with wild-type CCR5. A new study reports sustained HIV remission in a male who underwent allo-HSCT with cells from a donor with wild-type CCR5 and has not received ART for 32 months. The individual was diagnosed with an extramedullary myeloid tumour and received allo-HSCT along with the immunosuppressive compound ruxolitinib. The authors reported that after ART interruption, plasma viral loads remained undetectable. Moreover, they did not detect any evidence of intact proviruses or replication-competent viruses. No virus could be amplified in CD4+ T cell cultures that were expanded after allo-HSCT, but the cells could be infected with the virus in vitro. Finally, the authors report the lack of HIV-specific T cells and waning HIV-specific antibody levels. The factors underlying the lack of viral rebound remain to be determined, but the authors speculate allogeneic immunity and immunosuppressive drugs could have a role.