It has been proposed that blocking the PD-1/PD-L1 pathway with ICIs increases the production of antibodies against the hemidesmosomal protein BP180; an imbalance among autoreactive Th cells, Tregs, and T-cell-independent activation of TLRs may trigger the release of autoantibodies, with tumor expression of the BP180 antigen supporting the production of anti-BP180 antibodies [152–154]. Here, CD274 is linked to neoplasm.