This study provides evidence that chronic CS stimulates the accumulation of a COPD-relevant squamous and pro-inflammatory basal cell phenotype, most likely in response to smoke-induced injury which is supported by an impaired epithelial barrier integrity and increased expression of wound repair associated markers (KRT6A, FN1, VIM) including EREG by this basal cell subset [69,70,71]. This evidence concerns the gene KRT6A and chronic obstructive pulmonary disease.