Chlamydia trachomatis, an obligate intracellular pathogen, employs various mechanisms to manipulate host cell functions for its survival and replication. One significant study identified the Chlamydia effector Dre1, which binds to the dynactin complex, facilitating the repositioning of host organelles during infection. This interaction is crucial for nutrient acquisition and evasion of host immune responses, marking Dre1 as the first bacterial effector known to modulate dynactin function (ref: Sherry doi.org/10.1016/j.celrep.2025.115509/). Additionally, research on the divisome complex in Chlamydia revealed that FtsK is essential for the assembly of this unique structure, which is critical for cell division in FtsZ-less bacteria. The study utilized HeLa cell models to elucidate the localization patterns of divisome components, providing insights into the molecular mechanisms governing chlamydial division (ref: Harpring doi.org/10.7554/eLife.104199/). Furthermore, a novel mechanism was uncovered where Chlamydia induces ferroptosis in host cells to facilitate progeny release, highlighting the pathogen's ability to manipulate host cell death pathways for its reproductive success (ref: Chen doi.org/10.1371/journal.ppat.1013060/). These findings collectively enhance our understanding of Chlamydia's pathogenesis and its interactions with host cells, revealing potential targets for therapeutic intervention.