The finding of very high levels of miR-216b in prom1-exo, coupled with undetectable levels in parental FEMX-I cells, is intriguing in light of reports that miR-216b suppresses tumor growth and invasion by targeting KRAS in nasopharyngeal carcinoma [43] and inhibits cell proliferation and colony formation through Ras inhibition in a pancreatic cancer model [44]. The gene discussed is KRAS; the disease is neoplasm.