CDK4/6 is regarded as a promising target in treating LSCC when appropriate candidate patients are identified by the downstream functional assessment.38 Recent studies have found that inhibition of CDK4/6 not only induces tumor cell-cycle arrest, but also increases T-cell inflammatory signature in tumors, which may act synergistically with ICB therapies479,480 (Fig. 6b). This evidence concerns the gene CDK4 and neoplasm.