Analysis of tumor progression within MYC/Runx2 mice infected neonatally with MLV that maintain the IN TP- genotype as well as the integration preferences of such mutants in human K562 cells highlights the preferential integration into quiescent states and the strong selective pressure on MLV to maintain the IN tail peptide, through either internal deletions or recombination with endogenous retroviruses. The gene discussed is MYC; the disease is neoplasm.