Multiple studies have suggested the existence of direct or indirect crosstalk between TGF-β signaling and PI3K/Akt signaling, so we wonder whether PI3K/Akt pathway is also involved in NSCLC aggressiveness in the presence of miR-181b-mediated TGFβR1 inactivation. Here, TGFBR1 is linked to non-small cell lung carcinoma.