3.1. Genes and Pathways Responsible for the Action
The signaling pathways analyzed by DMA are as follows (see Kiyama & Zhu [13]; Kiyama et al. [183]): MAPK (such as G protein–coupled receptor (GPCR)/MAPK, MAPK/c-Jun N-terminal kinase (JNK), and NF-κB/MAPK/ERK) and other (such as angiogenesis, ErbB/human epidermal growth factor receptor (HER), nuclear receptor, and ubiquitin/proteasome) signaling pathways, or apoptosis pathways (such as those for death receptor, infectious response, and p53-dependent apoptosis), autophagy pathways (such as those for phosphatidylinositol-3-kinase (PI3K)/Akt/mTOR signaling and starvation stress response), cell cycle/DNA damage pathways (such as G1/S checkpoint and G2/M DNA damage checkpoint signaling pathways), cellular metabolism pathways (such as AMP-activated protein kinase (AMPK) and insulin receptor signaling pathways), chromatin/epigenetic regulation pathways (such as those for DNA methylation, heterochromatin, and histone modification), cytoskeletal regulation and adhesion pathways (such as those related to actin, adherens junction, and microtubule dynamics), development and differentiation pathways (such as hedgehog, Notch, TGF-β, and Wnt/β-catenin signaling pathways), immunology and inflammation pathways (such as those for B-cell receptor signaling, cytokine receptor signaling, inflammatory response, rheumatoid arthritis, T-cell activation, and TLR-induced immune response), neuroscience pathways (such as Alzheimer’s disease- and Parkinson’s disease-related signaling pathways) and translational control pathways (such as eIF2, eIF4/P70S6K, and mTOR signaling pathways). 
Since genes and pathways responsible for the action of TCM are related to various cell functions, it is almost impossible to understand the mechanisms of action just by studying the mixture of chemicals. There are cases in which effective chemicals (such as those shown in Table 2) were analyzed in order to understand specific mechanisms, such as Bax signaling/apoptosis (2,4,3′,5′-tetramethoxystilbene), ERK signaling/anti-atherosclerosis (brefeldin A), ERK signaling/anti-carcinogenesis (grifolin), estrogen signaling (ginsenosides F1/Rb1/Rg1/Rh1 and glycyrrhizin), estrogen signaling/carcinogenesis (3,3′-diindolylmethane), HSP70 (a 70 kilodalton heat shock protein) signaling/anti-carcinogenesis (paeoniflorin), NF-κB signaling/anti-carcinogenesis (quercetin), NF-κB signaling/anti-inflammation (ergosterol peroxide), NF-κB signaling/apoptosis (tanshinone IIA), NF-κB signaling/hypoxia (paeonol), Nrf2-antioxidant response element (ARE) signaling/chemoprevention (myricetin), PI3K-Akt signaling/chemoprevention (sulforaphane), PPAR-γ signaling/adipogenesis (aculeatin), reactive oxygen species (ROS) signaling/apoptosis (β-hydroxyisovalerylshikonin), Rho/ROCK signaling/cell migration (tanshinone IIA), skn-1 signaling/life-span extension (diallyl trisulfide), and tumor necrosis factor receptor 1 (TNFR1)-IGF-1R signaling/apoptosis (emodin). These signaling pathways are summarized in Figure 1.