In this study, we demonstrated that the SPHK1/PBX1 axis induced the activation of cyclin-dependent kinases, thereby promoting NSCLC tumorigenicity in vitro and in vivo, which was in agreement with a previous study showing that the overexpression of PBX1 in HF-MSCs promoted the progression of the cell cycle from G0/G1 to the S phase [43]. The gene discussed is PBX1; the disease is hydrops fetalis.