A potentially interesting connection for MOAP-1-dependent tumor suppression is the link to DNA damage control by expression changes in PARP1 and PARP3 (key players involved in the detection and repair of DNA double strand breaks), ATM (a DNA damage checkpoint kinase), ATR-interacting protein, and the catalytic subunit of DNA-activated protein kinase (DNA-PK, a DNA damage sensor) (Tables 2 and 3). The gene discussed is PRKDC; the disease is neoplasm.