Interestingly, two studies in CRC reported that miR-200b-3p stimulates tumor growth by targeting CDKN1B and negatively regulating p27/kip1 in TGFBR2-null CRC [40], and miR-200b-3p overexpression promotes CRC cell proliferation by targeting reversion-inducing cysteine-rich protein with Kazal motifs (RECK) [20]. The gene discussed is RECK; the disease is neoplasm.