For example, we previously reported that the oral administration of the celecoxib derivative DMC (4‐ [5-(2,5-dimethylphenyl)-3 trifluoromethyl-1H-pyrazol-1-yl]-benzene-sulfonamide) resulted in inhibition of P-Akt and ultimately suppressed development of prostate tumours [34]. The gene discussed is AKT1; the disease is prostate neoplasm.