Simlialy, Pontel et al. [91] reported FSP1-epigenetic silencing in both T- and B-ALL, in which the promoter of the gene coding for FSP1 is hypermethylated, silencing the expression of FSP1 and creating a selective dependency on GSH-centered anti-ferroptosis defenses, this metabolic vulnerability that might be of therapeutic interest in ALL. The gene discussed is AIFM2; the disease is acute lymphoblastic leukemia.