Considering that the biological functions and underlying mechanisms of SLC34A2 in CRC is poorly understood, we, here, demonstrated that SLC34A2-induced up-regulation of EZH2 expression promoted the proliferation of CRC cells and their cisplatin resistance to apoptosis in vivo and in vitro, which implied that EZH2 also could serve as the target of potential therapeutics. The gene discussed is SLC34A2; the disease is colorectal carcinoma.