Thus, our objectives were that, in plasma samples from LC patients with and without COPD, the following mechanisms were explored: (1) expression levels of microRNAs known to be involved in lung carcinogenesis; (2) redox balance, prooxidant and antioxidant markers; (3) VEGF and TGF-beta 1 protein levels; (4) relationships between clinical and biological variables; and (5) potential associations between expression levels of microRNAs and those of oxidative stress and inflammatory cytokines. This evidence concerns the gene TGFB1 and laryngotracheoesophageal cleft.