Notably, patients with MDS who possess particular somatic mutations, such as those in the TP53, ASXL1, SETBP1, TET2, SRSF2, and RUNX1 genes, have an increased propensity to react favourably to PD-1/PD-L1 inhibitors (Chien et al., 2021) confirming that many cellular and molecular mechanisms, known to promote cellular senescence, including alteration of the splicing machinery, are crucial stimulators of the expression of the PD-L1 protein. The gene discussed is TP53; the disease is myelodysplastic syndrome.