Here we interrogated if specific inhibition of MCL-1 and BCL-2, using combinations of these inhibitors that are efficacious in mouse cancer models and have advanced to clinical trials or are FDA-approved for cancer therapy [11,16–19] would: 1) limit M.tb burden in human macrophages more than inhibition of just one target, 2) limit growth of both drug susceptible and resistant M.tb stains, 3) further reduce M.tb burden when combined with front line antibiotics INH or RIF, and 4) limit M.tb growth in a pre-clinical human in vitro granuloma model, which we previously developed [20]. This evidence concerns the gene MCL1 and cancer.