For instance, Maryjka et al. described a gastroesophageal junction collision tumor in which the esophageal component demonstrated mismatch repair deficiency with loss of MLH1 and PMS2, whereas the gastric component exhibited distinct, nonoverlapping molecular alterations, including an EML4::ALK fusion and intact mismatch repair status, confirming two independent neoplasms [24]. The gene discussed is EML4; the disease is neoplasm.