Since B cells also express immune checkpoint molecules such as CTLA-4, PD-1, and PD-L1 [43–46] that may negatively regulate BCR signaling [47], and since treatment with CTLA-4 or PD-1 inhibitors has been associated with increase in certain autoimmune antibodies [48, 49], it is possible that immune checkpoint inhibitors may enhance activation of B cells and overall contribute to either anti-tumor response (memory B cells) and/or development of autoimmunity [50]. The gene discussed is CTLA4; the disease is neoplasm.