Except for the common immune response pathways shared with IPF and COPD (antigen presentation by MHC class II molecules, B cell signaling, and T cell co-signaling receptors), silica exposure in silicosis may specifically drive antigen presentation by MHC class I molecules, which are recognized by CD8 + T cells, leading to damage to pulmonary epithelial cells through cytotoxic pathways, followed by pulmonary fibrosis (Zhang and Zhang, 2020). The gene discussed is CD8A; the disease is silicosis.