Our analysis of the effect of AUF-1 loss on the steady state and mRNA stability of selected validated targets was based on the hypothesis that the documented AUF1 loss – ex vivo, in COPD’s bronchiolar epithelium, or in vitro by cytomix – would be functionally reflected by the changes, brought by cell activation, in the AUF-1 targets identified by RIP-seq. The gene discussed is HNRNPD; the disease is chronic obstructive pulmonary disease.