And, multiple strategies targeting Mcl-1, including small molecule BH3 mimetics (Kotschy et al. 2016) synthetic peptides fit into Mcl-1 BH3-binding groove (Stewart et al. 2010), covalent allosteric inhibition (Akcay et al. 2016), proteolysis targeting chimera (PROTAC) mediated Mcl-1 degradation (Wang et al. 2019), interfering Mcl-1 transcription (Thomas et al. 2013), have been proved to possess promising anti-cancer efficiency. This evidence concerns the gene MCL1 and cancer.