An increasing number of studies are exploring the noncatalytic functions of enzymes in addition to their catalytic activity.[35] Here, we demonstrated that the destruction of KAT6A LLPS, rather than catalytic inhibition, increased PARP1 trapping and restored sensitivity to PARPi, providing potential therapeutic strategies for PARPi‐resistant ovarian cancer. The gene discussed is PARP1; the disease is ovarian carcinoma.