Selective IKKB knockdown with CRIPSR/Cas9 technology in the patient-derived MSCs demonstrated reduced pro-inflammatory secretome from the deactivation of inflammatory effector (e.g., IKKB and NF-κB), which, in turn, increased survival and immuno-potency in atherosclerosis- and T2DM-patient MSCs. The gene discussed is IKBKB; the disease is type 2 diabetes mellitus.