ALDH1A1 detoxifies the active form of Cyclophosphamide to an inactive metabolite. Treatment causes an NF-κB–IL-6–dependent inflammatory environment that induces stemness. Loss of PPARγ causes expansion of the CSC population resistant to cyclophosphamide. Mortalin (mtHsp70) upregulation leads to an increase in stem cell markers such as OCT4 and ALDH1 leading to drug resistance. Treatment-induced senescence greatly enhanced tumor stemness and relapse potential upon exit from the senescence state through the Wnt pathway. The gene discussed is NFKB1; the disease is neoplasm.