Successful cell division requires chromosomes to be separated on opposite sides of the cell. This is achieved by depolymerisation of kinetochore fibers and spindle elongation. Forces required for spindle elongation in human cells are linked to sliding of antiparallel microtubules and sliding capacity has been demonstrated in vitro for multiple motor proteins, but the molecular mechanism of sliding during anaphase in the spindles of human cells remains unknown. Here I show, by using combined depletion and inactivation assays to explore redundancy between multiple targets together with CRISPR technology, that PRC1-dependent motor KIF4A/kinesin-4, together with EG5/kinesin-5 motor is essential for spindle elongation in human cells. Depletion of KIF4A, or its partner PRC1, together with EG5 inhibition, completely arrests cell division in early anaphase while depletion of other PRC1-interacting partners had minor effect on anaphase progression. On the other hand, decreased stability of midzone microtubules measured by photoactivation assay or their structural changes studied by expansion microscopy cannot explain the observed anaphase arrest. Conclusively, my work demonstrates that two independent sliding modules power sliding mechanism that drives anaphase spindle elongation in human cells thus resolving longstanding question in the field and bridging the gap between extensive in vitro work on sliding motors and their concrete actions within the cell.