There was higher expression of APOM in NSCLC tissues than in non‐NSCLS and of APOM overexpression promoted invasion and proliferation of NSCLC cells in vitro and tumor growth in vivo by upregulating expression of S1PR1 and activating the PI3K/AKT and ERK1/2 signaling pathways.84 This evidence concerns the gene S1PR1 and non-small cell lung carcinoma.