Similarly, another meta-analytic study focusing on CDKN2A, which encodes the p16 protein [58] and which acts as a key tumor suppressor by inhibiting cyclin-dependent kinases, thereby enforcing cell cycle arrest at the G1 phase, revealed that increased expression of p16 is also significantly linked to a higher risk of malignant transformation (RR = 2.01, 95% CI = 1.36 to 2.96; p < 0.001) [43], suggesting a possible compensatory upregulation in response to oncogenic stress or disrupted regulatory circuits. This evidence concerns the gene CDKN2A and neoplasm.