Increased collagen in lung cancer tissues can also bind to leukocyte-associated immunoglobulin-like receptor 1 (LAIR-1), which induces protein tyrosine phosphatase SHP-1-mediated T cell exhaustion, whereas inhibition of LOXL2 reduces tumor collagen deposition, increases CD8+ T cell infiltration, and the sensitivity of anti-PD-1/PD-L1 therapy [77]. The gene discussed is CD8A; the disease is neoplasm.