ALK and neoplasm: Although traditional targetable genetic driver mutations in Anaplastic Lymphoma Kinase (ALK) and Epidermal Growth Factor Receptor (EGRR) are observed as low levels in SC (3), the growing body of literature with respect to SC supports that higher programmed death ligand-1 (PD-L1) expression and tumor mutational burden (TMB) are common (4, 5), which represent higher response rates and potentially survival benefits under immune checkpoint inhibitor (ICI) treatment, especially PD-L1 inhibitors (6).