In conjunction with the latter and research on oesophageal tumours [64] and non-small cell lung cancer [65], our data suggest that activation of receptor tyrosine kinase signalling and acquired inhibitor vulnerability may be an early adaptation mechanism of response to CDK4/6 inhibitors, which could persist in fully resistant cancers but opens up the possibility of targeting CDK4/6 inhibitor resistance with inhibitors of receptor tyrosine kinase signalling cascades. The gene discussed is CDK4; the disease is non-small cell lung carcinoma.