The interplay of VCAN with its EGF-like domain, p53, and CDKN1A has been shown to be dependent on oncogenic mutations in EGFR. When EGFR is mutated, the ligand EGF facilitates an unexpected upregulation of the originally tumor-suppressing gene CDKN1A, which enables further cell proliferation and tumor progression [45,46]. This evidence concerns the gene VCAN and neoplasm.