Given that the Mcm4 mutant mice are tumor prone, yet are not subjected to external stresses for DNA replication that stall forks, one might ask why there is evidence of stalled forks in such mouse cells.[21] Even more relevant, one might also ask why human tumors do not seem to arise with underlying mutations in Mcm genes that weaken reserve MCM hexamers, display similar stalled forks, and produce genomic instability subjected to selection pressure at the cellular level that results in tumorigenesis. This evidence concerns the gene MCM4 and neoplasm.