INSL5 and Epstein-Barr virus infection: Li et al. reported that EBV infection of nasopharyngeal epithelial cells led to the upregulation of INSL5 expression, and INSL5 and its receptor GPCR142 axis promoted the expression of genes related to glycolysis by activating the intracellular STAT5 signaling pathway, thus affecting the reprogramming of cellular glucose metabolism and promoting the proliferation and metastasis of nasopharyngeal carcinoma 29.