Recently, we reported a similar cell population expressing CD49a, CD49b and Eomes in mouse tumour models, and this was found to represent an intermediate population between TGFβ‐mediated conversion of cNK cells into ILC1s.46 Whether this plasticity between cNKs and ILC1s also occurs in malaria remains unknown but perturbation of TGFβ signalling following infection could help explain the disparity between ILC1 and NK cell frequencies after PcAS infection. The gene discussed is ITGA2; the disease is neoplasm.