Indeed, TAM receptors have been shown to favour the escape of tumour cells from immune surveillance by activating innate immune checkpoints and, in particular, by upregulating PD-L1 expression.33,34 Our transcriptomic analysis upon TYRO3 depletion revealed no modulation of CD274 (PD-L1) expression, but a significant increase in TNFSF9 (CD137L) expression. This evidence concerns the gene CD274 and neoplasm.