PRC1 and cancer: 2024). Specifically, a 24-h depletion of the PRC1 subunit PH results in irreversible activation of key members of the JAK–STAT pathway, which in turn trigger a switch to a self-sustaining cancer cell fate, even upon restoration of normal PRC1 activity (Parreno et al. 2024). These EICs are proficient in DSB repair and do not show chromosome rearrangements or major increase in the mutational load (Parreno et al. 2024).