Given that apoptotic cell death is increased in COPD and in response to cigarette smoke as well as in the SARS-CoV-2 infection [59,72,73], it is possible that cleaved HuR expression in smoker and COPD-derived cells is driving an apoptotic phenotype and consequent lung damage in these diseases. Here, ELAVL1 is linked to chronic obstructive pulmonary disease.