The loss of HLA heterozygosity is a focal diminishing of the ability to present neoantigens to facilitate immune evasion and subclonal genome evolution, which is under strong microenvironmental selection pressures later in tumor evolution; this occurs in 40% of NSCLC patients and is associated with a high subclonal neoantigen burden, APOBEC-mediated mutagenesis, upregulation of cytolytic activity, and PD-L1 positivity [209]. Here, CD274 is linked to neoplasm.