The novel finding of cytomix-triggered increase in β-galactosidase staining, of amplitude similar to the one induced by etoposide, suggests that the concurrent loss of AUF-1 is contributing to cytomix-induced cellular senescence, supporting the role of this RBP in inflammatory and accelerated senescence responses in COPD, as initially suggested by Auf1-/- mice phenotype and further supported by the presence of enhanced DNA damage in AUF-1 silenced cells (47). This evidence concerns the gene HNRNPD and chronic obstructive pulmonary disease.