We report three important findings, 1) sensitivity of NSCLC cell lines to MCL-1 inhibition was independent of MCL-1 expression and driver mutation status in these cells, 2) the combined inhibition of MCL-1 and BCL-2/xL with maritoclax and navitoclax (ABT263) is superior to either single drug treatment, especially in erlotinib-resistant EGFR mutated NSCLC cells, and 3) phosphorylated AKT is a marker for sensitivity to the maritoclax and navitoclax combination therapy. Here, BCL2 is linked to non-small cell lung carcinoma.