Our model shows that these three factors do not work independently, but PTBP1 represses MCL1 expression by facilitating miR-101 targeting to MCL1. Therefore, while therapeutics acting on these three factors are still under development, it is necessary to consider the crosstalk between PTBP1, MCL1, and miR-101 in order to best deploy the resulting molecules for optimized impact in treating cancer patients. This evidence concerns the gene MCL1 and cancer.