DNA replication and transcription must be intricately coordinated as both machineries navigate the same chromatin landscape to ensure genome stability and proper cell function. Here, we show that altering their elongation rates—specifically, slowed transcriptional elongation alongside rapid replication fork progression—does not elicit replicative stress. Instead, this independent kinetic variation accelerates the acquisition of naive pluripotency during in vitro dedifferentiation, revealing an u