Some sweet corn (Zea mays L.) hybrids and inbreds can be severely injured by applications of postemergence herbicides. An association was observed between the responses of sweet corn hybrids and inbreds to nicosulfuron and mesotrione, and F2 families derived from a cross of a sensitive (Cr1) and a tolerant (Cr2) sweet corn inbred segregated for response to these two herbicides. These observations prompted us to examine the inheritance of sensitivity in sweet corn to multiple postemergence herbicide treatments with different modes of action and to determine if there was a common genetic basis for cross-sensitivity to these herbicides. The sensitive and tolerant inbreds, progeny in the F1, F2, BC1, and BC2 generations, and BC1S1, BC2S1, F2:3 (S1:2) and F3:4 (S2:3) families were screened for responses to eight herbicide treatments. Based on segregation of tolerant and sensitive progeny and segregation of family responses, our data indicate that a single recessive gene in Cr1 conditioned sensitivity to four acetolactate synthase (ALS)-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), a 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba + diflufenzopyr), and a protoporphyrinogen oxidase (PPO)-inhibiting herbicide (carfentrazone). Based on highly significant positive correlations of phenotypic responses among BC1S1, BC2S1, F2:3, and F3:4 families, the same gene (or closely linked genes) appeared to condition responses to each of these herbicide treatments. The dominant allele also conditions tolerance to bentazon [a photosystem II (PSII)-inhibiting herbicide] although another gene(s) also appeared to affect bentazon tolerance.