In MYB-NFIB-positive and PI3KC-amplified patient-derived ACC, the PI3K inhibitor alpelisib increased the activity of cisplatin in vivo by suppression of MYB levels; however, stronger tumor growth inhibition and MYB downregulation were observed in MYB-NFIB and PIK3CAR88Q constitutively active mutant ACC in combination with RA[164]. This evidence concerns the gene NFIB and neoplasm.