Objective: To describe the behavior of the BCL-2 protein in non-small-cell lung cancer cell models in response to treatment with ALK (anaplastic lymphoma kinase) protein tyrosine kinase inhibitors (crizotinib and alectinib) and their potential dual BCL-2-ALK inhibition. Materials and methods: Three non-small-cell-lung cancer cell models were used: Ba/f3 EML4-ALKWT, Ba/f3 EML4-ALKL1196M and Ba/f3 EML4-ALKG1202R, generated by site-directed mutagenesis. These were treated with crizotinib and alectinib in a dose-responsive manner, and an apoptosis assay was also conducted to confirm pharmacological susceptibility. Subsequently, BCL-2 protein expression was measured under three treatment conditions (no treatment, 100 nM crizotinib and 50 nM alectinib). Finally, a search for BCL-2 and ALK ligands was performed for molecular docking simulation and interaction energy calculation, measured in kca...