Conversely, however, high baseline activation of an RTK-dependent pathway (e.g. an IGF1R-AKT axis in liposarcoma cells) does not preclude induction of senescence following CDK4/6 inhibitor monotherapy [41, 44], and ultimately, mechanisms of CDK4/6 inhibitor resistance may be distinct in cells capable of achieving the senescent phenotype. This evidence concerns the gene IGF1R and liposarcoma.