Moreover, what is already known about the antineoplastic capabilities of celecoxib in melanoma, independent from COX-2/prostaglandin E2 (PgE2) inhibition, is that it suppresses cancer cell growth and promotes apoptosis via Wnt/β-catenin and m-TOR (mechanistic target of rapamycin) substitutive pathway inhibition, and reduces the epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and the signal transducer and activator of transcription 3 (STAT3) expression [25,26,27,28]. The gene discussed is MTOR; the disease is cancer.