Our data further indicate that CILK1 offers an alternative way for tumor cells to maintain the activation status of ERK1/2, as evidenced by the facts that only the treatment of MEK1/2 inhibitor in CILK1-silencing cells completely blocked the phosphorylation of ERK1/2, and over-expression of CILK1 was able to partially rescue the inhibition of phospho-ERK1/2 in the presence of MEK1/2 inhibitor. The gene discussed is CILK1; the disease is neoplasm.