Our data demonstrated that overexpression of FHL1 inhibited the proliferation, colony formation potential, and caused cell-cycle G1 arrest of HN-13 by apoptosis induction whereas ablating FHL1 promoted the proliferation, the colony formation potential and G1-S transition of HN-4 and SCC-25, suggesting FHL1 acts as a tumor suppressor in HNSCCs. Here, FHL1 is linked to neoplasm.