The important role of PAFR in oral cancer was also confirmed by the study of Kohei Kawasaki et al. Cisplatin in combination with ginkgolide B inhibited PAFR and the phosphorylation levels of its downstream signaling pathways ERK and Akt, and promoted the expression of cleaved caspase-3, leading to apoptosis and increasing the sensitivity of oral cancer cells to cisplatin treatment [60]. Here, CASP3 is linked to lip and oral cavity carcinoma.