As chromosome mis-segregation generally generates a cell cycle arrest and chromosome gains or losses of larger chromosomes commonly function as tumor suppressors (Duijf et al., 2013; Santaguida et al., 2017; Sheltzer et al., 2017), and in particular a loss of MSH2 does not confer a direct proliferative advantage to the cells, we provided MSH2-deficient cells a selective advantage by exposure to the methylating agent Temozolomide (TMZ). Here, MSH2 is linked to neoplasm.