Moreover, in mice xenografts, derived from SGC7901 cells, treatment with a specific inhibitor of this enzyme induced reduction of H3K79 di-methylation (H3K79me2), expression of CDK4 and CDK6, cyclin-dependent kinases involved in the regulation of G1 to S transition, and tumor size, suggesting that DOT1L promote cell cycle progression by H3K79 di-methylation in CDK4 and CDK6 genes (Song et al., 2020). The gene discussed is DOT1L; the disease is neoplasm.