MARK1 and neoplasm: Since CCL5 was reported to rapidly induce cyclin D1, c-Myc, Ha-Ras through MARK-ERK, and Jak/STAT signaling, as well as glucose in-take and ATP production to stimulate tumor growth (Ding et al., 2016; D. ; Gao & Fish, 2018; Murooka, Rahbar, & Fish, 2009), the HNSCC cell lines with the high expression of the four chemokines were sensitive to the anti-tumor drug targeting MARK-ERK and RAS pathways.