Therefore, a conceivable framework of the molecular mechanism of thrombin-induced lung cancer cell Glc-82 function could be as follows: thrombin activates PAR1 on the cell membrane; the activated PAR1 transfers some signal to downregulate PTEN expression; the negative regulation of PTEN on PI3K is attenuated, which activates the AKT signaling pathway and changes the expression of Skp2 and p27; finally, the cell function is affected by AKT signaling pathway. This evidence concerns the gene AKT1 and lung carcinoma.