Ras mutations drive tumorigenesis yet persist in normal tissues. Elliot et al. explore this paradox, finding that HRASG12V induces bifurcating cell fates in the zebrafish larval epidermis, with lamc2+krt18+ cancer stem cell-like cells emerging from permissive cells at the preneoplastic stage and expressing neutrophil-modulating cytokines that instigate reciprocal tumor-supportive crosstalk.