Since POLQ over-expression might not provide a selective advantage for HR-proficient cells survival in the absence of external stress, we postulated that upregulation of Polθ could be selected during tumorigenesis in order to adapt to high levels of endogenous or external replicative stress, a condition that characterizes many cancers (Macheret and Halazonetis, 2015). Here, POLQ is linked to cancer.