Recent studies indicate that agrin provides stimulatory signals to augment focal adhesion kinase (FAK) activity during cancer growth and invasion.9, 42 FAK induces cell cycle progression through cyclin D1, involving extracellular-signal-regulated kinase (ERK), among others.43 In OSCC cells, treatment with agrin shRNA reduced the levels of FAK and ERK phosphorylated forms, as well as reduced the expression of cyclin D1 (Fig. 2d). This evidence concerns the gene CCND1 and cancer.