Based on the anti-tumor effect of the COX-pathway, many preclinical studies have indicated that the treatment by inhibiting COX-2 (key component of COX-pathway) and a receptor tyrosine kinase such as EGFR, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2), could yield additive effect, which is far more effective than either single agent alone [33–35]. The gene discussed is NTRK1; the disease is neoplasm.