After infection of nodule host cells, Rhizobium bacteria differentiate into nitrogen fixing bacteroids. Depending on the host plant, this process can be reversible or alternatively terminal, after which bacteria can no longer replicate. Terminal bacteroid differentiation is controlled by the host plant and was first described in Medicago truncatula and other legumes in the inverted repeat-lacking clade to be dependent on a group of nodule-specific, cysteine-rich (NCR) peptides. Recent publications have shown that NCR-like peptides can also be found in other clades of legumes and that the host's armory of NCR peptides defines shape and degree of bacteroid differentiation. Terminal bacteroid differentiation is associated with a block of the bacterial cell division machinery and profound regulatory changes in the bacterial cell cycle. Several bacterial genes and proteins have been found to be of key importance for establishing a successful symbiotic interaction with NCR-producing hosts. The bacterial BacA protein was the first protein to be identified to be essential for bacterial survival within the host cell upon NCR challenge in IRLC legumes. However, recent studies have highlighted that BacA appears to be not essential for symbiosis with all NCR-producing legumes and alternative mechanisms can protect bacteria from NCR peptides. Particularly, rhizobia can actively promote the degradation of NCR peptides and thus escape terminal bacteroid differentiation, tilting the symbiotic relationship in their favor. Our understanding of the complex interlinked relationships of the NCR peptide imposed stop of bacterial replication and the mechanisms that rhizobia have evolved to survive and counter host restrictions is still only beginning. Here, we aim to give an overview on our current understanding of this symbiotic tug of war.