CTLA4 and plasma cell myeloma: Although anti-myeloma effector responses seem to be efficiently primed, they subsequently fail as myeloma cells are able to circumvent T-cell effector functions through an array of mechanisms, such as defects in cytokine secretion, loss of proliferative capacity, impaired cytotoxicity, altered activity of transcription factors such as T-bet or the expression of immune checkpoint inhibitors (ICIs), including PD-1, CTLA-4, or TIGIT [70].