Several researchers have proposed various molecular mechanisms such as enhancement of the proinflammatory factors c-Jun N-terminal kinase/Activator protein-1, NF-κB, and phosphoinositide 3-kinases, phosphorylation of double-stranded RNA-activated protein kinase, and oxidative stress-mediated signaling in ER stress and the UPR pathway associated with lung diseases [30,31,32,33,34,35,36]. This evidence concerns the gene EIF2AK2 and lung disorder.