TP53 and colorectal carcinoma: Amounts of surface-exposed PS were independent from (I) molecular CRC subtype, i.e. chromosomal/microsatellite instability or CpG-island and methylator phenotype, that have been found to impede drug response [25, 26]; (II) the corresponding mutational profile (i.e. K-ras, B-raf, p53, APC status); or (III) clinicopathological parameters (gender, age, TNM stage).