In another scenario, if the clonal population that was selected after CRISPR/Cas9 OPN-knockout happened to be clone MT-3 and its orthotopic tumor penetrance was compared to that of the parental Met-1 population, then one could erroneously interpret the necessity of OPN for primary tumor formation, when in fact this clone, prior to OPN knockout, already inherently forms tumors with lower incidence (~66%) than the parental population (100%) (Figs 1B and 3B). Here, SPP1 is linked to neoplasm.