Namely, through the application of: i) the RNA-Seq workflow we confirmed the overexpression of pro-survival TP63 in subset #8 CLL patients compared to #6 subset (Papakonstantinou et al., 2019), and ii) the ChIP-Seq workflow we confirmed the non-canonical, differential binding of EZH2 to the promoter of IGF1R, whose expression is non-canonically induced in U-CLL patients by EZH2-recruited MYC leading to the activation of the PI3K pathway (Kosalai et al., 2019). The gene discussed is EZH2; the disease is B-cell chronic lymphocytic leukemia.