HRAS and neoplasm: Our finding suggests that the expression of Nrf2E79Q early during promotion may create a favorable environment for the expansion of keratinocytes with non-canonical mutations in Kras and Hras. According to the Ras sweet-spot model [45], if RAS signaling and/or levels are too low, tumors will not develop, and if Ras expression/signaling are too high, senescence and apoptosis can occur blocking tumor development.