Hence, dormancy-promoting ECM biomolecules released in the dormant tumor cell’s microenvironment direct p38 pathway activation in the early-stage tumor cell–ECM crosstalk [4,64], increasing INK4 and Cip/Kip family proteins, CDKIs, and E2F transcriptional inhibition via the MAPK/TGFb2 pathway to inhibit CDK4/6 and Cyclin-CDK complexes to arrest tumor cells in the G0-G1 phase [58]. The gene discussed is MAPK1; the disease is neoplasm.