PAR2 can transactivate EGFR (Kawao et al., 2005; Huang et al., 2013; Michel et al., 2014), and P2pal-18S as a PAR2 inhibitor cooperatively augmented gefitinib to attenuate phosphorylation of EGFR in both gefitinib-sensitive and -resistant NSCLC cells (Figures 1D,H), which suggested that the inhibition of receptor transactivation may affect drug resistance. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.