Key biological effects include: Replication stress tolerance through impaired CHK1 phosphorylation (CHK1 being an ATR-regulated essential kinase), leading to accumulated DNA damage and subsequent tumor cell apoptosis (13); Homologous recombination deficiency caused by BARD1 mutations disrupting BRCA1 complex function and H2A-K15ub modification dynamics (14). Here, CHEK1 is linked to neoplasm.