SULT2B1b depletion was reported to promote AKR1C3 expression, which activates extracellular-signal-regulated kinase 1/2 (ERK1/2) tumor cell survival signal, activates androgen receptors, and induces epithelial-to-mesenchymal (EMT)-like changes that promote cancer progression and invasiveness (Park et al., 2020). This evidence concerns the gene AKR1C3 and cancer.