A few well documented CNVs were identified in HNSCC that included amplification of 3q27.3q28 (CLDN1), 7q11.1q31.31 (LAMB1), 8q11.23q24.3 (MYC and PTK2), 11q13.2q22.3 (PPFIA1, CTTN, FGF3, FGF4, FADD, CCND1, MMP7, MMP20, MMP27, MMP8, MMP10, MMP1, MMP3, MMP12, and MMP13), and deletion of 1p21.1p11.2 (COL11A1 and GSTM3), 3p14.2 (FHIT), 3p26.1 (GRM7), 3p13 (FOXP1), 9p21.3 (CDKN2A and CDKN2B), and 18q12.1q23 (SERPINB2) [56–61], all of which were involved in tumor cell proliferation and angiogenesis in oral carcinogenesis [50, 62–65]. This evidence concerns the gene CLDN1 and neoplasm.