Lastly, in the genetic context of TP53-R248Q, only the siRNA-mediated AKR1C3 knockdown was found to significantly abrogate the promotion of proliferation (Fig. 6M), independent viability (Fig. 6N), migration (Fig. 6O), invasion (Fig. 6P), together with the xenograft tumor growth in vivo (Fig. 6Q) and its associated Ki-67 expression (Fig. 6R) by FOSB overexpression in NSCLC cells. Here, AKR1C3 is linked to neoplasm.