Xu et al. (2018b) have found that DPP-resistant gastric cancer cell lines, such as BGC823/DDP cells and SGC7901/DDP cells secrete more CCL2 to maintain DDP resistance. It has further been found that CCL2 overexpression increases the expression of p62 by activating PI3K/AKT/mTOR signaling pathway, whilst the increased expression of p62, in turn, activates the transcription of CCL2, inhibits autophagy, and forms a positive feedback loop to maintain drug resistance (Xu et al., 2018b). The gene discussed is AKT1; the disease is gastric cancer.