Although Yang et al. also reported divergent effects of DEC and ROM on apoptosis-related genes in metastatic human colon carcinoma cells (47), the impact of these substances on other cancer entities appeared to be cancer-type specific: ROM treatment induced G2/M phase arrest and apoptosis via activation of ERK-MAPK and JNK-MAPK pathways in hepatocellular cancer (48), while ROM induced apoptosis in non-small cell lung cancer cells by inhibition of RAF-MEK-ERK PI3K/AKT signaling and by downregulation of anti-apoptotic genes and upregulation of the pro-apoptotic BAX (49). The gene discussed is BAX; the disease is cancer.