TP53 and neoplasm: We next evaluated genomic aberrations in cell cycle and senescence machinery genes (CDKN1A, CDKN1B, CDKN2A, CDKN2B, CDKN2D, RB1 and TP53) using the aforementioned NGS panel on the basis of the hypothesis that myeloid-targeted approaches may depend on cell arrest and associated senescence programs in tumour cells for response.