Given how rapidly CDK4/6 inhibition induces transcriptional programming, it is possible that even a once-off treatment of CDK4/6i given upfront with BRAFi+MEKi would be sufficient to enhance the quality of the anti-tumor T cell response initiated by BRAFi-MEKi, without disrupting immune-potentiating myeloid populations or compromising ongoing CTL expansion. Here, CDK4 is linked to neoplasm.