In this regard, a study over 514 ALM samples identified that these tumours frequently display a dysregulated CDK4 pathway, a product of either gains of CDK4/CCND1 or loss of CDKN2A that, in turn, promote G1 to S cell cycle transition and thus contribute to tumour proliferation (Kong et al., 2017) (Figure 3). This evidence concerns the gene CCND1 and neoplasm.