As some research suggested that loss of SPHK1 was critical to p53-dependent tumor suppression mechanism, and SPHK1 inhibition combined with p53 overexpression played an important role in inducing cell death35,36; however, in our work, the expression level of p53 seemed to be little affected by different POTEE expression (Supplementary Fig. 5a), which indicated POTEE-mediated SPHK1 changes was independent of p53 status. Here, POTEE is linked to neoplasm.