These associations were independent of NSCLC genetic drivers and correlates of immune infiltration, including tumor purity, tumor-infiltrating neutrophils, and the proportion of myeloid cells (Fig S14B–D).28 We further recapitulated these associations using an alternative metric of TI-CH that estimates the fraction of non-tumor cells harboring CHIP mutations (Supp Methods, Fig S14E). The gene discussed is C4B; the disease is neoplasm.