Given the relative tumor suppressive influence of the C57BL/6 background [55–57], one could anticipate to observe further tumor types upon Rassf10 loss, like we report here for human patients, in other mouse strains or in combination with other tumor suppressors or even in an oncogenic background (e.g., KRAS), which might be addressed by others in the future. The gene discussed is KRAS; the disease is neoplasm.