AKR1C2 and non-small cell lung carcinoma: This result is consistent with our prior findings: 1) the canonical enzymatic activity is dispensable for AKR1C1 in promoting NSCLC metastasis; 2) the two paralogues of AKR1C1, namely, AKR1C2 and AKR1C3, although possessing similar catalytic activities and biological functions 15, 16, 33, yet minimally contribute to the malignancy of NSCLC 10.