RAD9A and cancer: Therefore, it seems plausible to assume that stochastic or adverse exposure events during early (intrauterine and postnatal) development may increase cancer susceptibility through epigenetic reprogramming (Marshall et al., 2014[56]; Walker and Ho et al., 2012[70]), including epimutations of RAD9A. We identified 5 patients (four 1N and one 2N) with ≥ 10 % mean RAD9A methylation in mosaic in intron 2 and using DBS analysis we could show that the mosaic epimutations represent ≥ 2 % hypermethylated alleles.