In 2014, Hountis et al. introduced a dual role concept for S100A2 in lung cancer, implicating that S100A2 is primarily expressed in the nucleus at an early stage of NSCLC, where it mediates resistance to p53-dependent apoptosis and inhibits tumour-promoting genes (e.g., PA1-1 and vimentin) and in later stages relocates to the cytoplasm in a Ca2+-dependent manner [114]. The gene discussed is S100A2; the disease is neoplasm.