Strong indications exist that an AML-negative disease course is associated with the deregulation of cellular responses to oxidative stress; the enzyme 8-oxoguanine DNA glycosylase1 (OGG1) mutant S326C that provides extended support to NFκB transcriptional activity was observed more frequently in patients who experienced AML relapse, and these patients exhibited a shorter relapse-free survival rate [17]. The gene discussed is NFKB1; the disease is acute myeloid leukemia.