As tumor formation in these models involves either continuous or repeated replication stress and DNA damage during compensatory proliferation, respectively35, 42, we propose that CHK1 exerts “oncogenic” potential under these conditions in lymphocytes, while it may well act as a haploinsufficient tumor suppressor in the mammary gland, the skin or on a Chk2-deficient background24, 46. This evidence concerns the gene CHEK2 and neoplasm.