EDNRA and neoplasm: In support of this hypothesis, our data show that PARPi-unresposive cells, exhibiting a greater expression of ETAR compared to the parental counterpart, regain PARPi sensitivity upon ETAR depletion, suggesting that the aberrant activation of the ETAR-driven signalling may function as an escape route through which tumour cells evade PARPi therapy engaging an adaptive mechanism to survive.