Since Mcl-1 silencing has been found to elicit tumor regression and cell death in various cancer models [52], including B-CLL [53], our data provide the rationale for further evaluating the use of Met-DCA cocrystal (also in combination with the Bcl-2 specific targeting drug venetoclax) for the treatment of B-CLL, also in virtue of the potential anti-leukemic activity of Met-DCA independently of the p53 status. The gene discussed is MCL1; the disease is neoplasm.