Specifically, loss of TP53-mediated repression or RB1/E2F dysregulation can increase the expression of platelet-derived growth factor receptor alpha (PDGFRα), a receptor tyrosine kinase that promotes proliferation, angiogenesis, and stromal recruitment and is overexpressed in a significant proportion of OSA cases; CSPG4 has been implicated in potentiating PDGFRα signaling through ligand presentation [31,32]. Here, CSPG4 is linked to obstructive sleep apnea syndrome.