To bring the proof of concept that HSP90 inhibition could be a pertinent strategy to induce CMA in hematological malignancies, Allende-Vega et al. established that, under stress conditions induced by Dichloroacetate, a PDK1 inhibitor, 17-Allylamino Geldanamycin (17-AAG), a Geldanamycin derivative used in the clinic, favors the degradation of the mutant form of TP53 (R248Q) through CMA in AML cell lines [100]. The gene discussed is TP53; the disease is acute myeloid leukemia.