· Reduces the frequency of non-homologous end joining (NHEJ) and increases the efficiency of homology-directed repair (HDR) in CRISPR-Cas9 genome editing (Robert et al.).
· Inhibits tumor growth and sensitizes human cancer cells to DNA double-strand-break (DSB)-inducing therapies (chemo- or radio-therapy) by inhibiting both DNA-PK and PI3K and preventing the execution of DSB repair (Chen et al.; Dietlein et al.; Munck et al.).
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