For example, genetic or epigenetic silencing of BMAL1 and/or CLOCK has been shown to increase tumor proliferation or growth rates in hematologic cancer [71], colon cancer [72], pancreatic cancer [73], tongue squamous cell carcinoma (TSCC) [74], breast cancer [75], lung adenocarcinoma [18], hepatocellular carcinoma (HCC) [76], nasopharyngeal carcinoma (NPC) [77], and glioblastoma multiforme (GBM) [78]. Here, BMAL1 is linked to neoplasm.