Root-knot and cyst nematodes are biotrophic parasites that invade the root apex of host plants and migrate toward the vascular cylinder where they cause the differentiation of root cells into galls (or root-knots) containing hypertrophied multinucleated giant-feeding cells, or syncytia, respectively. The precise molecular mechanisms that drive the formation of such unique nematode feeding sites are still far-off from being completely understood. The diverse gene expression changes occurring within the host cells suggest that both types of plant-parasitic nematodes modulate a variety of plant processes. Induction and repression of genes belonging to the host cell cycle control machinery seem to be essential to drive the formation of such specialized nematode feeding cells. We demonstrate that nematodes usurp key components regulating the endocycle in their favor. This is illustrated by the involvement of anaphase-promoting complex (APC) genes (CCS52A and CCS52B), the endocycle repressor DP-E2F-like (E2F/DEL1) gene and the ROOT HAIRLESS 1 PROTEIN (RHL1), which is part of a multiprotein complex of the toposiomerase VI, in the proper formation of nematode feeding sites. Altering the expression of these genes in Arabidopsis plants by down- or overexpressing strategies strongly influences the extent of endoreduplication in both types of nematode feeding site leading to a disturbance of the nematode's life cycle and reproduction.