According to a published data, eIF6 silencing not only obviously induces CASP3-dependent apoptosis in NSCLC cells but also elevates SA--Gal activity and p21 levels, which is not conducive to the induction of cellular senescence pathways [45], suggesting that eIF6 might have initiated cell death, but this effect are prevented because of effector CASP3 inhibition, thereby cells emit persistent mitogen signaling and develop into an excessive proliferating population. This evidence concerns the gene GAL and non-small cell lung carcinoma.