Blocking ICOSL had a significant impact on the anti-tumor efficacy of both BI 853520 + anti-OX40 and BI 853520 + anti-4-1BB (Figure 6L,M), suggesting that enhanced T-cell expression of ICOS may be an important mechanism through which a FAK inhibitor can potentiate the anti-tumor activity of anti-OX40 and anti-4-1BB targeted therapies. The gene discussed is CACNA1A; the disease is neoplasm.