English: (A) Reassembly of histone H3/H4 heterodimers at replication forks is mediated by the sequential actions of the chromatin assembly factors ASF1 and CAF1. New histones carry H4K5ac/H4K12ac predisposition marks, which are required for their nuclear import. ASF1 can bind both new and evicted histones, ensuring tightly controlled histone recycling and nucleosome reassembly; (B) Replication stress interferes with the restoration of epigenetic information at stalled forks. Fork arrest results in excessive histone eviction and accumulation of ASF1 loaded with both old and new histones. Fork restart triggers rapid nucleosome assembly, which can result in unbalanced incorporation of old and new histones. Replication stress also promotes the accumulation of the H3K9me1 pre-deposition mark, which may serve as a template for H3K9me3 and HP1-mediated heterochromatin formation. Finally, impaired HDAC function may affect the removal of pre-deposition acetyl-marks, causing epigenetic changes in post-replication chromatin. Together, these defects have the potential to either promote or inhibit the expression of nearby genes.^[1]