In addition to p53-related aspects, the resistance to cancer treatment in CLL has been connected to biochemical alterations targeting membrane transporters, deoxycytidine kinase, and cytoplasmic 5'-nucleotidase cN-II activities, and more recently to changes in the levels of miR-34a [7], a miRNA belonging to the class of small non-coding RNA molecules mediating post-transcriptional gene silencing. The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.