A preparation of human allogeneic T-lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-BCMA CAR T-cells CTX120 recognize and bind to BCMA-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of BCMA-positive tumor cells. BCMA, a receptor for proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. The disruption of endogenous TCR prevents graft-versus-host disease (GvHD). The disruption of MHC class I molecules increases the persistence of the CAR T-cells.