In addition, the phosphorylation of nucleosomal H2AX by DNA‐PK facilitates FACT‐induced dissociation of H2AX, while ADP‐ribosylation of SPT16 promotes the dissociation of FACT from the nucleosome, which leads to the stabilization of nucleosomal H2AX.[27] But whether this proposed mechanism exactly exists in tumor cells treated with DNA‐damage agents remains unclear. The gene discussed is PRKDC; the disease is neoplasm.