RB1 and cancer: As both CDKN2C and RB1 interact with G1/S cell cycle checkpoint through CDK4/6 [27–29], they are potentially targetable through CDK4/6 inhibition [30], for which it has been shown in other cancers that co-deletion of CDKN2C and CDKN2A with functional presence of RB1 increases sensitivity in cell lines [31].